Lists of words, usually in alphabetical order, giving information about form, pronunciation, etymology, grammar, and meaning.
The new and thickened layer of scar tissue that forms on a PROSTHESIS, or as a result of vessel injury especially following ANGIOPLASTY or stent placement.
The innermost layer of an artery or vein, made up of one layer of endothelial cells and supported by an internal elastic lamina.
Cells contained in the bone marrow including fat cells (see ADIPOCYTES); STROMAL CELLS; MEGAKARYOCYTES; and the immediate precursors of most blood cells.
Relatively undifferentiated cells that retain the ability to divide and proliferate throughout postnatal life to provide progenitor cells that can differentiate into specialized cells.
A high-molecular-weight plasma protein, produced by endothelial cells and megakaryocytes, that is part of the factor VIII/von Willebrand factor complex. The von Willebrand factor has receptors for collagen, platelets, and ristocetin activity as well as the immunologically distinct antigenic determinants. It functions in adhesion of platelets to collagen and hemostatic plug formation. The prolonged bleeding time in VON WILLEBRAND DISEASES is due to the deficiency of this factor.
Protein analogs and derivatives of the Aequorea victoria green fluorescent protein that emit light (FLUORESCENCE) when excited with ULTRAVIOLET RAYS. They are used in REPORTER GENES in doing GENETIC TECHNIQUES. Numerous mutants have been made to emit other colors or be sensitive to pH.
Myosin type II isoforms found in smooth muscle.
The larger subunits of MYOSINS. The heavy chains have a molecular weight of about 230 kDa and each heavy chain is usually associated with a dissimilar pair of MYOSIN LIGHT CHAINS. The heavy chains possess actin-binding and ATPase activity.
A ureahydrolase that catalyzes the hydrolysis of arginine or canavanine to yield L-ornithine (ORNITHINE) and urea. Deficiency of this enzyme causes HYPERARGININEMIA. EC 3.5.3.1.
Damages to the CAROTID ARTERIES caused either by blunt force or penetrating trauma, such as CRANIOCEREBRAL TRAUMA; THORACIC INJURIES; and NECK INJURIES. Damaged carotid arteries can lead to CAROTID ARTERY THROMBOSIS; CAROTID-CAVERNOUS SINUS FISTULA; pseudoaneurysm formation; and INTERNAL CAROTID ARTERY DISSECTION. (From Am J Forensic Med Pathol 1997, 18:251; J Trauma 1994, 37:473)
Either of the two principal arteries on both sides of the neck that supply blood to the head and neck; each divides into two branches, the internal carotid artery and the external carotid artery.
A rare autosomal recessive disorder of the urea cycle. It is caused by a deficiency of the hepatic enzyme ARGINASE. Arginine is elevated in the blood and cerebrospinal fluid, and periodic HYPERAMMONEMIA may occur. Disease onset is usually in infancy or early childhood. Clinical manifestations include seizures, microcephaly, progressive mental impairment, hypotonia, ataxia, spastic diplegia, and quadriparesis. (From Hum Genet 1993 Mar;91(1):1-5; Menkes, Textbook of Child Neurology, 5th ed, p51)
An essential amino acid that is physiologically active in the L-form.
Use or insertion of a tubular device into a duct, blood vessel, hollow organ, or body cavity for injecting or withdrawing fluids for diagnostic or therapeutic purposes. It differs from INTUBATION in that the tube here is used to restore or maintain patency in obstructions.
A broad category of receptor-like proteins that may play a role in transcriptional-regulation in the CELL NUCLEUS. Many of these proteins are similar in structure to known NUCLEAR RECEPTORS but appear to lack a functional ligand-binding domain, while in other cases the specific ligands have yet to be identified.
The nonstriated involuntary muscle tissue of blood vessels.
The symptom of paroxysmal pain consequent to MYOCARDIAL ISCHEMIA usually of distinctive character, location and radiation. It is thought to be provoked by a transient stressful situation during which the oxygen requirements of the MYOCARDIUM exceed that supplied by the CORONARY CIRCULATION.
Drugs or agents which antagonize or impair any mechanism leading to blood platelet aggregation, whether during the phases of activation and shape change or following the dense-granule release reaction and stimulation of the prostaglandin-thromboxane system.
Dilation of an occluded coronary artery (or arteries) by means of a balloon catheter to restore myocardial blood supply.
A family of percutaneous techniques that are used to manage CORONARY OCCLUSION, including standard balloon angioplasty (PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY), the placement of intracoronary STENTS, and atheroablative technologies (e.g., ATHERECTOMY; ENDARTERECTOMY; THROMBECTOMY; PERCUTANEOUS TRANSLUMINAL LASER ANGIOPLASTY). PTCA was the dominant form of PCI, before the widespread use of stenting.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
An effective inhibitor of platelet aggregation commonly used in the placement of STENTS in CORONARY ARTERIES.
Devices that provide support for tubular structures that are being anastomosed or for body cavities during skin grafting.
Proteolytic enzymes from the serine endopeptidase family found in normal blood and urine. Specifically, Kallikreins are potent vasodilators and hypotensives and increase vascular permeability and affect smooth muscle. They act as infertility agents in men. Three forms are recognized, PLASMA KALLIKREIN (EC 3.4.21.34), TISSUE KALLIKREIN (EC 3.4.21.35), and PROSTATE-SPECIFIC ANTIGEN (EC 3.4.21.77).
A family of trypsin-like SERINE ENDOPEPTIDASES that are expressed in a variety of cell types including human prostate epithelial cells. They are formed from tissue prokallikrein by action with TRYPSIN. They are highly similar to PROSTATE-SPECIFIC ANTIGEN.
A generic term used to describe a group of polypeptides with related chemical structures and pharmacological properties that are widely distributed in nature. These peptides are AUTACOIDS that act locally to produce pain, vasodilatation, increased vascular permeability, and the synthesis of prostaglandins. Thus, they comprise a subset of the large number of mediators that contribute to the inflammatory response. (From Goodman and Gilman's The Pharmacologic Basis of Therapeutics, 8th ed, p588)
Cell surface proteins that bind ATRIAL NATRIURETIC FACTOR with high affinity and trigger intracellular changes influencing the behavior of cells. They contain intrinsic guanylyl cyclase activity.
A potent natriuretic and vasodilatory peptide or mixture of different-sized low molecular weight PEPTIDES derived from a common precursor and secreted mainly by the HEART ATRIUM. All these peptides share a sequence of about 20 AMINO ACIDS.
A PEPTIDE of 22 amino acids, derived mainly from cells of VASCULAR ENDOTHELIUM. It is also found in the BRAIN, major endocrine glands, and other tissues. It shares structural homology with ATRIAL NATRIURETIC FACTOR. It has vasorelaxant activity thus is important in the regulation of vascular tone and blood flow. Several high molecular weight forms containing the 22 amino acids have been identified.
The hearing and equilibrium system of the body. It consists of three parts: the EXTERNAL EAR, the MIDDLE EAR, and the INNER EAR. Sound waves are transmitted through this organ where vibration is transduced to nerve signals that pass through the ACOUSTIC NERVE to the CENTRAL NERVOUS SYSTEM. The inner ear also contains the vestibular organ that maintains equilibrium by transducing signals to the VESTIBULAR NERVE.
The outer part of the hearing system of the body. It includes the shell-like EAR AURICLE which collects sound, and the EXTERNAL EAR CANAL, the TYMPANIC MEMBRANE, and the EXTERNAL EAR CARTILAGES.
A PEPTIDE that is secreted by the BRAIN and the HEART ATRIA, stored mainly in cardiac ventricular MYOCARDIUM. It can cause NATRIURESIS; DIURESIS; VASODILATION; and inhibits secretion of RENIN and ALDOSTERONE. It improves heart function. It contains 32 AMINO ACIDS.
A protein factor that regulates the length of R-actin. It is chemically similar, but immunochemically distinguishable from actin.
A large class of structurally-related proteins that contain one or more LIM zinc finger domains. Many of the proteins in this class are involved in intracellular signaling processes and mediate their effects via LIM domain protein-protein interactions. The name LIM is derived from the first three proteins in which the motif was found: LIN-11, Isl1 and Mec-3.
A zinc-binding phosphoprotein that concentrates at focal adhesions and along the actin cytoskeleton. Zyxin has an N-terminal proline-rich domain and three LIM domains in its C-terminal half.
The parts of a transcript of a split GENE remaining after the INTRONS are removed. They are spliced together to become a MESSENGER RNA or other functional RNA.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
The main trunk of the systemic arteries.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
A class of protein components which can be found in several lipoproteins including HIGH-DENSITY LIPOPROTEINS; VERY-LOW-DENSITY LIPOPROTEINS; and CHYLOMICRONS. Synthesized in most organs, Apo E is important in the global transport of lipids and cholesterol throughout the body. Apo E is also a ligand for LDL receptors (RECEPTORS, LDL) that mediates the binding, internalization, and catabolism of lipoprotein particles in cells. There are several allelic isoforms (such as E2, E3, and E4). Deficiency or defects in Apo E are causes of HYPERLIPOPROTEINEMIA TYPE III.
Thickening and loss of elasticity of the walls of ARTERIES of all sizes. There are many forms classified by the types of lesions and arteries involved, such as ATHEROSCLEROSIS with fatty lesions in the ARTERIAL INTIMA of medium and large muscular arteries.

Recombinant human interleukin-10 inhibits proliferation of vascular smooth muscle cells stimulated by advanced glycation end products and neointima hyperplasia after carotid injury in the rat. (1/339)

The purposes of this study was to determine the effects of recombinant human interleukin-10 (rhIL-10) on proliferation of vascular smooth muscle cells (VSMCs) stimulated by advanced glycation end products (AGE) and neointima hyperplasia after rat carotid arterial injury. Rat aortic VSMCs were cultured and treated with rhIL-10 or AGE respectively, and then co-treated with rhIL-10 and AGE. Proliferation of VSMCs was quantified by colormetric assay. Cell cycle analysis was performed by flow cytomertry. Sprague-Dawley rats were treated with recombinant human IL-10 (rhIL-10) for 3 d after carotid arteries injury. The ratio of neointima to media area at the site of arterial injury was measured 28 d after balloon injury. The p44/42 MAPK activity was evaluated by the immunoblotting technique using anti-p44/42 phospho-MAPK antibody. Compared to control, AGE stimulated VSMCs proliferation. rhIL-10 alone had no effect on VSMCs growth. With AGE stimulation, rhIL-10, at dose as low as 10 ng/ml, inhibited VSMCs growth (P<0.05). The cell number in G(0)/G(1) phase of AGE and rhIL-10 co-treatment group was higher than that of AGE treatment alone (P<0.01) by flow cytometry analysis. Compared with the control group of neointima hyperplasia in rats, the ratio of neointima to media area of recombinant human IL-10 group was reduced by 45% (P<0.01). The p44/42 MAPK activity was significantly enhanced by AGE. The AGE effects were opposed by rhIL-10. The anti-inflammatory cytokine rhIL-10 inhibits AGE-induced VSMCs proliferation. Recombinant human IL-10 also inhibited neointima hyperplasia after carotid artery injury in rats. The results suggest the possibility that recombinant human IL-10, as a potential therapeutic approach, prevents neointimal hyperplasia.  (+info)

Novel neointimal formation over sirolimus-eluting stents identified by coronary angioscopy and optical coherence tomography. (2/339)

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A case of a newly developed yellow neointima at stent implanted site 1 year after sirolimus-eluting stent placement: angioscopic findings. (3/339)

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Effect of alpha lipoic acid in a porcine in-stent restenosis model. (4/339)

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Blockade of TGF-beta by catheter-based local intravascular gene delivery does not alter the in-stent neointimal response, but enhances inflammation in pig coronary arteries. (5/339)

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A20 inhibits post-angioplasty restenosis by blocking macrophage trafficking and decreasing adventitial neovascularization. (6/339)

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Local arterial nanoparticle delivery of siRNA for NOX2 knockdown to prevent restenosis in an atherosclerotic rat model. (7/339)

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Mechanisms of vein graft adaptation to the arterial circulation: insights into the neointimal algorithm and management strategies. (8/339)

For patients with coronary artery disease or limb ischemia, placement of a vein graft as a conduit for a bypass is an important and generally durable strategy among the options for arterial reconstructive surgery. Vein grafts adapt to the arterial environment, and the limited formation of intimal hyperplasia in the vein graft wall is thought to be an important component of successful vein graft adaptation. However, it is also known that abnormal, or uncontrolled, adaptation may lead to abnormal vessel wall remodeling with excessive neointimal hyperplasia, and ultimately vein graft failure and clinical complications. Therefore, understanding the venous-specific pathophysiological and molecular mechanisms of vein graft adaptation are important for clinical vein graft management. Of particular importance, it is currently unknown whether there exist several specific distinct molecular differences in the venous mechanisms of adaptation that are distinct from arterial post-injury responses; in particular, the participation of the venous determinant Eph-B4 and the vascular protective molecule Nogo-B may be involved in mechanisms of vessel remodeling specific to the vein. This review describes (1) venous biology from embryonic development to the mature quiescent state, (2) sequential pathologies of vein graft neointima formation, and (3) novel candidates for strategies of vein graft management. Scientific inquiry into venous-specific adaptation mechanisms will ultimately provide improvements in vein graft clinical outcomes.  (+info)

TY - JOUR. T1 - Deletion of Krüppel-like factor 4 in endothelial and hematopoietic cells enhances neointimal formation following vascular injury.. AU - Yoshida, Tadashi. AU - Yamashita, Maho. AU - Horimai, Chihiro. AU - Hayashi, Matsuhiko. PY - 2014. Y1 - 2014. N2 - Krüppel-like factor 4 (Klf4) is involved in a variety of cellular functions by activating or repressing the transcription of multiple genes. Results of previous studies showed that tamoxifen-inducible global deletion of the Klf4 gene in mice accelerated neointimal formation following vascular injury, in part via enhanced proliferation of smooth muscle cells (SMCs). Because Klf4 is also expressed in non-SMCs including endothelial cells (ECs), we determined if Tie2 promoter-dependent deletion of Klf4 in ECs and hematopoietic cells affected injury-induced neointimal formation. Klf4 conditional knockout (cKO) mice were generated by breeding Tie2-Cre mice and Klf4 floxed mice, and their phenotype was analyzed after carotid ligation ...
Heterogeneous neointima were detected in 21.5% of DES-treated lesions in the study population. The occurrence of neointimal tissue in this group was significantly associated with both advanced age and initial clinical presentation of acute coronary syndrome. MACE occurred more frequently in patients in the heterogeneous group compared with those in the nonheterogeneous group during the average 31-month follow-up period (13.7% vs. 2.9% in the homogeneous group vs. 7.3% in the layered group, p = 0.001). In addition, we found that inclusion in the heterogeneous group and minimal lumen CSA on follow-up OCT examination were independent risk factors for future MACE. To the best of our knowledge, this is the first study to investigate the clinical significance of neointimal tissue patterns without features of neoatherosclerosis. Our data suggest that the heterogeneous neointimal tissue pattern is correlated with poor long-term clinical outcomes.. OCT is a valuable intravascular imaging modality for ...
It has been shown that angiotensinII receptor blocker (ARB) has an inhibitory effect on neointima formation. Bone marrow-derived mononuclear cells (BM-MNCs) which express angiotensinII (AngII) type 1 receptor (AT1R) have been shown to give rise to smooth muscle(SM) like cells at injured vascular walls. However, the role of AngII in the process of BM-MNC incorporation to neointimal formation is little known. Human peripheral blood mononuclear cells (PB-MNCs) were cultured in the presence of PDGF-BB and basic FGF. Immunohistochemistry and RT-PCR revealed that PB-MNCs gave rise to SM-like cells. Immunohistochemistry revealed that αSMA, SM1 and SMemb become positive in PB-MNC derived SM-like cells. RT-PCR confirmed the expression of αSMA, SMemb and AT1R mRNA in PB-MNC derived SM- like cells. The number of SM-like progenitor cells were increased by AngII, and this was blocked by an ARB CV-11974(αSMA+cell/ HPF: 32.6±3.3, 23.4±2.3 vs. 19.0±2.0, P,0.001). CV-11974 alone further decreased the ...
The goal of this project is to define the role of peroxisome proliferator-activated receptor (PPAR)3 activation in neointima formation. Neointima formation occu...
Based on our previous results implicating CaMKIIδ2 as regulator of cell migration and proliferation in cultured rat aortic VSM cells,16,18 we investigated the function of CaMKIIδ2 in the vascular response to injury. Consistent with results using an in vitro system,18 we observed a rapid and marked modulation in vascular wall CaMKII isoform expression after balloon injury in vivo, coinciding with acquisition of a migratory/proliferative phenotype in both carotid artery medial VSM and adventitial fibroblasts. Inhibiting acute upregulation of the CaMKIIδ2 isoform attenuated migration and proliferation, and functionally suppressed neointima formation and adventitial thickening. We conclude from these studies that CaMKIIδ isoforms specifically couple Ca2+ signals to regulate cell migration and proliferation, and that increased expression of these isoforms in VSM or adventitial myofibroblasts is an important component of injury induced vascular wall remodeling.. Potential sources of neointimal VSM ...
OSU Libraries and Press Research Data Services provides guidance and support for all aspects of the research data lifecycle, from planning your data management strategy during the proposal phase through preserving your data at the conclusion of your project. Our services are free of charge, and we are happy to partner with you on proposals and projects. Our guide to Research Data Services offers support for managing data, creating and maintaining metadata and documentation, and services for data sharing and preservation.. ...
OBJECTIVES: We used optical coherence tomography, which has a resolution of |20 microm, to analyze thin layers of neointima in rapamycin-eluting coronary stents. BACKGROUND: Lack of neointimal coverage has been implicated in the pathogenesis of drug-eluting coronary stent thrombosis. Angiography and intracoronary ultrasound lack the resolution to examine this. METHODS: We conducted a randomized trial in patients receiving polymer-coated rapamycin-eluting stents (Cypher, Cordis, Johnson & Johnson, Miami, Florida) and nonpolymer rapamycin-eluting stents (Yukon, Translumina, Hechingen, Germany) to examine neointimal thickness, stent strut coverage, and protrusion at 90 days. Twenty-four patients (n = 12 for each group) underwent stent deployment and invasive follow-up at 90 days with optical coherence tomography. The primary end point was binary stent strut coverage. Coprimary end points were neointimal thickness and stent strut luminal protrusion. RESULTS: No patient had angiographic restenosis. For
TY - JOUR. T1 - The APOSTEL recommendations for reporting quantitative optical coherence tomography studies. AU - Cruz-Herranz, Andrés. AU - Balk, Lisanne J.. AU - Oberwahrenbrock, Timm. AU - Saidha, Shiv. AU - Martinez-Lapiscina, Elena H.. AU - Lagreze, Wolf A.. AU - Schuman, Joel S.. AU - Villoslada, Pablo. AU - Calabresi, Peter. AU - Balcer, Laura. AU - Petzold, Axel. AU - Green, Ari J.. AU - Paul, Friedemann. AU - Brandt, Alexander U.. AU - Albrecht, Philipp. PY - 2016/6/14. Y1 - 2016/6/14. N2 - Objective: To develop consensus recommendations for reporting of quantitative optical coherence tomography (OCT) study results. Methods: A panel of experienced OCT researchers (including 11 neurologists, 2 ophthalmologists, and 2 neuroscientists) discussed requirements for performing and reporting quantitative analyses of retinal morphology and developed a list of initial recommendations based on experience and previous studies. The list of recommendations was subsequently revised during several ...
OCT data analysis was performed offline using proprietary software (LightLab Imaging Inc.). Analysis of angiographic images, quantitative coronary angiography (Medis, Leiden, the Netherlands), and OCT was performed by experienced investigators (P.B. and P.M.). Regarding blinding, the very different presentation of the 2 stent types (including, in particular, the hub of the devices and the angiographic appearances of the markers) made it impractical to blind the operators; however, for the angiographic and OCT analysis, investigators were blinded to the randomization arm. The analyst was blinded to all clinical and procedural variables and thus, did not have any knowledge of stent sizes or stent type. When a strut was felt to be malapposed, the distance from the strut to lumen surface was recorded. Only after completion of the analysis was the stent type used to then confirm the presence or absence of malapposition by incorporating the actual strut thickness for the 2 stents used. This is ...
The question of whether DES are safe, has become an area of considerable interest and controversy with the publication of a relatively small randomized trial (BASKET-LATE), an observational study and a meta-analysis reporting increased rates of ST, MI, and death with DES compared to BMS. The motivating factor was the presentation of a meta-analysis at the European Society of Cardiology meeting in Barcelona in September 2006, which suggested an increase in the risk of death and MI following implantation of sirolimus-eluting stents.. The major issue in these meta-analyses is that they were limited either by small sample sizes, duration of follow-ups, lack of access to source data, or by using landmark analyses that excluded events in first 6 months.. Moreover, the largest meta-analysis of DES vs. BMS and SES vs. PES published recently in The Lancet by Settler et al performed a network analyses with a mixed-treatment comparison of 38 randomized trials (18023 patients) with a follow-up of up to 4 ...
Our study demonstrated that vulnerable plaque characteristics, including thinner fibrous cap, greater lipid arc, longer lipid core length, and TCFA, were seen more frequently in UAP culprit lesions with NV when compared with those without NV, but not in the non-culprit lesions of UAP and in the lesions of SAP.. In this study, we observed NV in 35% of the culprit lesions in UAP patients. This finding is consistent with the previous report by Kitabata et al,9 where NV was found in 38% of the culprit lesions in UAP patients. NV was observed in 34% of non-culprit lesions and in 28% of the lesions in SAP patients. The difference was not significant between the three groups. Our findings, which associate NV with the presence of TCFA, thinner fibrous cap, and larger plaque burden, are also in good agreement with the previous report.9 The results obtained from the study by Fujii K et al13 have shown that ruptured plaques in culprit lesions of patients with acute coronary syndromes have greater plaque ...
The aim of the APOSTEL recommendations is to provide a consistent basis for assisting authors in composing conclusive reports of studies utilizing quantitative retinal OCT, allowing relevant comparisons across and between studies, and helping readers, reviewers, and editors to evaluate these findings. Furthermore, by emphasizing details that are of importance in such reports, we hope to generally improve the quality of future investigations in this area. Defining the relevant parameters for reporting may prompt researchers to thoroughly consider these criteria during the initial stages of study design. Such an approach could help facilitate OCT research in centers intending to incorporate OCT for clinical trials or other research purposes. Adherence to the recommendations can help avoid common pitfalls in the design and reporting of OCT studies. These recommendations are not intended to impose a rigid format on reports of OCT-based research, but rather to provide suggestions and guidance on ...
Fibronectin-splice variant containing extra domain A (Fn-EDA) is associated with smooth muscle cells (SMCs) following vascular injury. The role of SMC-derived Fn-EDA in SMC phenotypic switching or its implication in neointimal hyperplasia remains unclear. Herein, using human coronary artery sections with a bare metal stent, we demonstrate the expression of Fn-EDA in the vicinity of SMC-rich neointima and peri-strut areas. In mice, Fn-EDA colocalizes with SMCs in the neointima of injured carotid arteries and promotes neointima formation in the comorbid condition of hyperlipidemia by potentiating SMC proliferation and migration. No sex-based differences were observed. Mechanistic studies suggested that Fn-EDA mediates integrin- and TLR4-dependent proliferation and migration through activation of FAK/Src and Akt1/mTOR signaling, respectively. Specific deletion of Fn-EDA in SMCs, but not in endothelial cells, reduced intimal hyperplasia and suppressed the SMC synthetic phenotype concomitant with ...
Background: Reendothelialization following vascular injury after balloon angioplasty or stent implantation is clinically extremely relevant to promote vascular healing and prevent fatal events such as stent thrombosis and restenosis. We already identified the importance of Toll-like receptor (TLR) 2/6 for endothelial regeneration. We now investigated the therapeutic potential of the TLR2/6 agonist MALP-2 on reendothelialization in a murine model of vascular injury. Methods and Results: The left common carotid artery of C57BL/6N mice was experimentally injured and reendothelialization was quantified by Evans Blue staining after 3 days in en face prepared vessels. A single intravenous injection of MALP-2 (1 or 10 µg) following vascular injury dose-dependently accelerated reendothelialization up to 3.5-fold (n=12-18, P,0.001) which was abolished by administration of neutralizing antibodies against TLR2 and TLR6. Proliferation of endothelial cells at the wound margins determined by ...
Neurofibromin 2 (NF2), a potent tumor suppressor, is reported to inhibit proliferation in several cell types. The role of NF2 in neointima hyperplasia after vascular injury is unknown. We explored the role of NF2 in proliferation, migration of vascular smooth muscle cell (VSMC) and neointima hyperplasia after vascular injury. NF2 phosphorylation was elevated in VSMC subjected to platelet-derived growth factor (PDGF)-BB and in artery subjected to vascular injury. Mice deficient for Nf2 in VSMC showed enhanced neointima hyperplasia after injury, increased proliferation and migration of VSMC after PDGF-BB treatment. Mechanistically, we observed increased nuclear p-NF2, declined p-Yes-Associated Protein (YAP), nuclear translocation of YAP after PDGF-BB treatment or injury. NF2 knockdown or YAP overexpression showed similar phenotype in VSMC proliferation, migration and neointima hyperplasia. YAP inhibition abolished the above effects mediated by NF2 knockdown. Finally, NF2 knockdown further promoted
Results All endovascular procedures and OCT pullback runs were feasible. Stent apposition was satisfactory on the immediate post-stent OCT reconstructions. At 12-week controls, all stents and jailed branches were patent. Mean neointimal thickness was 0.11±0.04 mm on the free segments of the stent. The mean ostia surface at 12 weeks was 319 750±345 533 μm2 with 3D-OCT reconstructions and 351 198±396 355 μm2 with SEM image-derived calculations. Good correlation was found for ostia surface values between the two techniques; the values did not differ significantly in this preliminary study. ...
DESIGN:. Imaging and vasomotion Substudy:. 50 consecutive patients enrolled in the COMPARE II trial at the University of Fribourg Medical Center will undergo follow-up re-angiography 14 months after index procedure with assessment of Optical coherence tomography (OCT) and vasomotion testing.. ENDPOINT SUBSTUDY (all at 14 months):. Primary endpoint imaging: percentage of uncovered stent struts per lesion and mean neointimal thickness assessed by OCT.. vasomotion: coronary vasomotion assessed with quantitative coronary angiography at rest and during supine bicycle exercise. ...
Our study addressed the question of whether or not expression of vWF influenced neointimal formation in arteries with altered shear stress. We found that the absence of vWF did not alter the size of the neointimal lesions, the number of layers of cells in the neointima, or the expression of PCNA in the neointima or media. The exact mechanism of neointimal formation in arteries with altered shear stress is unknown but is likely to be multifactorial. It has been known for some time that many forms of vascular manipulation will induce neointimal formation, and there appear to be important species-dependent responses (reviewed in References 30 through 3230 31 32 ). First, simple surgical isolation of an artery induces neointima in rabbits, and thus, either the operative procedure alone or the disturbed flow that likely occurs during healing contributes to neointimal hyperplasia.33 Second, vascular injury applied either externally to a rabbit artery or endoluminally in rats, rabbits, and pigs induces ...
Three-dimensional morphological response of lipid-rich coronary plaques to statin therapy: a serial optical coherence tomography study
Core2 1-6-N-glucosaminyltransferase-I deficiency protects injured arteries from neointima formation in ApoE-deficient mice. - Huan Wang, Weiyu Zhang, Rong Tang, Robert P Hebbel, M Anna Kowalska, Chunxiang Zhang, Jamey D Marth, Minoru Fukuda, Chuhong Zhu, Yuqing Huo
Medical definition of neointima: a new or thickened layer of arterial intima formed especially on a prosthesis or in atherosclerosis by migration and proliferation of cells from the media.
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While not always apparent, as the vehicle's mileage climbs, its strut mounts often deteriorate. Therefore, when the struts are being replaced (especially on high mileage vehicles), it's also the perfect time to replace the strut mounts in order to help restore the vehicle's like-new...
Neointimal hyperplasia refers to proliferation and migration of vascular smooth muscle cells primarily in the tunica intima, resulting in the thickening of arterial walls and decreased arterial lumen space. Neointimal hyperplasia is the major cause of restenosis after percutaneous coronary interventions such as stenting or angioplasty. The term neointima is used because the cells in the hyperplastic regions of the vascular wall have histological characteristics of both intima and normal artery cells. Neointimal hyperplasia first develops with damage to the arterial wall, followed by platelet aggregation at site of injury, recruitment of inflammatory cells, proliferation and migration of vascular smooth muscle cells, and collagen deposition. Mechanical injury of arterials due to stretching of arterial walls with a balloon catheter results in the recruitment of cells such as monocytes, macrophages, and neutrophils to the site of injury. Macrophages in particular express many growth factors, ...
Fibronectin-splice variant containing extra domain A (Fn-EDA) is associated with smooth muscle cells (SMCs) following vascular injury. The role of SMC-derived Fn-EDA in SMC phenotypic switching or its implication in neointimal hyperplasia remains unclear. Herein, using human coronary artery sections with a bare metal stent, we demonstrate the expression of Fn-EDA in the vicinity of SMC-rich neointima and peri-strut areas. In mice, Fn-EDA colocalizes with SMCs in the neointima of injured carotid arteries and promotes neointima formation in the comorbid condition of hyperlipidemia by potentiating SMC proliferation and migration. No sex-based differences were observed. Mechanistic studies suggested that Fn-EDA mediates integrin- and TLR4-dependent proliferation and migration through activation of FAK/Src and Akt1/mTOR signaling, respectively. Specific deletion of Fn-EDA in SMCs, but not in endothelial cells, reduced intimal hyperplasia and suppressed the SMC synthetic phenotype concomitant with ...
Fibronectin-splice variant containing extra domain A (Fn-EDA) is associated with smooth muscle cells (SMCs) following vascular injury. The role of SMC-derived Fn-EDA in SMC phenotypic switching or its implication in neointimal hyperplasia remains unclear. Herein, using human coronary artery sections with a bare metal stent, we demonstrate the expression of Fn-EDA in the vicinity of SMC-rich neointima and peri-strut areas. In mice, Fn-EDA colocalizes with SMCs in the neointima of injured carotid arteries and promotes neointima formation in the comorbid condition of hyperlipidemia by potentiating SMC proliferation and migration. No sex-based differences were observed. Mechanistic studies suggested that Fn-EDA mediates integrin- and TLR4-dependent proliferation and migration through activation of FAK/Src and Akt1/mTOR signaling, respectively. Specific deletion of Fn-EDA in SMCs, but not in endothelial cells, reduced intimal hyperplasia and suppressed the SMC synthetic phenotype concomitant with ...
Lipoprotein (a) level is associated with plaque vulnerability in patients with coronary artery disease: An optical coherence tomography study
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Bilirubin is a heme metabolite generated by the concerted action of the enzymes heme oxygenase and biliverdin reductase. Although long considered a toxic byproduct of heme catabolism, recent preclinical, and clinical studies indicate the bilirubin exerts beneficial effects in the circulation. In the present study, we determined whether local administration of bilirubin attenuates neointima formation following injury of rat carotid arteries. In addition, the ability of bilirubin to regulate the proliferation and migration of human arterial smooth muscle cells (SMCs) was investigated. Local perivascular administration of bilirubin immediately following balloon injury of rat carotid arteries significantly attenuated neointima formation. Bilirubin-mediated inhibition of neointimal thickening was associated with a significant decrease in ERK activity and cyclin D1 and A protein expression, and an increase in p21 and p53 protein expression in injured blood vessels. Treatment of human aortic SMCs with ...
TY - JOUR. T1 - Protective Aptitude of Annexin A1 in Arterial Neointima Formation in Atherosclerosis-Prone Mice-Brief Report. AU - de Jong, Renske J.. AU - Paulin, Nicole. AU - Lemnitzer, Patricia. AU - Viola, Joana R.. AU - Winter, Carla. AU - Ferraro, Bartolo. AU - Grommes, Jochen. AU - Weber, Christian. AU - Reutelingsperger, Chris. AU - Drechsler, Maik. AU - Soehnlein, Oliver. PY - 2017/2. Y1 - 2017/2. KW - annexin A1. KW - macrophage. KW - neointima formation. KW - resolution of inflammation. KW - INFLAMMATION. KW - RECRUITMENT. U2 - 10.1161/ATVBAHA.116.308744. DO - 10.1161/ATVBAHA.116.308744. M3 - Article. VL - 37. SP - 312. EP - 315. JO - Arteriosclerosis Thrombosis and Vascular Biology. JF - Arteriosclerosis Thrombosis and Vascular Biology. SN - 1079-5642. IS - 2. ER - ...
Fingerprint Dive into the research topics of Comparisons of the effects of stent eccentricity on the neointimal hyperplasia between Sirolimus-eluting stent versus Paclitaxel-eluting stent. Together they form a unique fingerprint. ...
B,Accumulating evidence shows that inhibition of the vascular renin-angiotensin system results in suppression of injury-elicited neointima formation. We attempted to determine whether or not combined treatment with an angiotensin II type 1 receptor blocker (ARB) and angiotensin converting enzyme inhibitor (ACEI) has an additive inhibitory effect on balloon-injury-elicited neointima formation in the carotid artery. Male Sprague-Dawley rats were treated with an ARB (valsartan: 3 mg/kg/day) and/or an ACEI (benazepril: 0.3 mg/kg/day) from 1 week before until 2 weeks after balloon injury. Experiments were also conducted with one-third of the dose combination used in the original experiments. Both ARB and ACEI inhibited neointima formation without any blood pressure changes. The full-dose combination lowered blood pressure and suppressed neointima formation significantly compared with the levels in the groups treated with either ACEI or ARB alone. The low-dose combination without blood pressure ...
Sigma-Aldrich offers abstracts and full-text articles by [Nick D Tsihlis, Muneera R Kapadia, Ashley K Vavra, Walker D Flannery, Christopher S Oustwani, Qun Jiang, Melina R Kibbe].
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Thank you for taking the time to nominate a fellow for TCTMDs Featured Fellow section on the Fellows Forum. Nominees should be current general or interventional cardiology fellows who you have supervised or mentored and think should be recognized for a combination of their scholarship, skills, talent, and commitment to top-notch patient care. If your nominee is selected, you will be notified of our selection and alerted when the story appears on TCTMD. Please email [email protected] with any questions ...
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Purpose: To determine the choroidal thickness (CT) profile in keratoconus (KC) patients using swept-source optical coherence tomography (SS-OCT). Methods: This was a prospective, cross-sectional study. One hundred two eyes of 52 KC patients were studied using Pentacam and SS-OCT. The macular CT profile was created by manually measuring the distance between the retinal pigment epithelium and the choroid-sclera junction on horizontal b-scans at nine different macular locations. The results were compared to 93 eyes of 93 healthy controls. Results: Mean age of the KC group was 34.9 ± 13.5 years and mean axial length (AL) was 24.1 ± 1.3 mm. Mean topographic KC classification (TKC) was 2.0; 39 eyes were classified as early KC (TKC ,1-2), 34 eyes as moderate (TKC 2, 2-3), and 29 as advanced (TKC 3+). Mean subfoveal CT was 383.2 μm in KC patients and 280.5 μm in control group (P , 0.001). CT in KC patients was statistically thicker in all measure locations (P , 0.001). CT in KC eyes decreased with ...
title: Optical coherence tomographic observation of morphological features of neointimal tissue after drug-eluting stent implantation., doi: 10.3349/ymj.2014.55.4.944, category: Article
ObjectiveIn balloon-injured rat carotid arteries, angiotensin-converting enzyme inhibitors (ACEI) decrease neointima formation, and a kinin receptor antagonist partially reverses this inhibitory effect. We studied which of the events leading to neointima formation are involved in the effects of ACEI
Principal Investigator:SAKUMA Makoto, Project Period (FY):1989 - 1990, Research Category:Grant-in-Aid for General Scientific Research (C), Research Field:General surgery
Technavio analysts forecast the global drug-eluting balloons market to grow to USD 664.35 million by 2021, at a CAGR of more than 27%.
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TY - JOUR. T1 - Longitudinal optical coherence tomography study of optic atrophy in secondary progressive multiple sclerosis. T2 - Results from a clinical trial cohort. AU - Winges, Kimberly. AU - Murchison, Charles F.. AU - Bourdette, Dennis. AU - Spain, Rebecca. PY - 2017/11/1. Y1 - 2017/11/1. N2 - Background: Limited prospective information exists regarding spectral-domain optical coherence tomography (SD-OCT) in secondary progressive multiple sclerosis (SPMS). Objective: Document cross-sectional and longitudinal retinal nerve fiber layer (RNFL) and macular ganglion cell plus inner plexiform layer (GCIPL) features of an SPMS clinical trial cohort. Methods: Prospective, observational study using a 2-year randomized placebo-controlled SPMS trial cohort with yearly SD-OCT testing. Post hoc analysis determined influences of optic neuritis (ON), disease duration, and baseline SD-OCT on annualized atrophy rates and on correlations between OCT and brain atrophy. Results: Mean RNFL and GCIPL values ...
TY - JOUR. T1 - ComparisOn of neointimal coVerage between zotaRolimus-eluting stent and everolimus-eluting stent using Optical Coherence Tomography (COVER OCT). AU - Kim, Jung Sun. AU - Kim, Byeong Kuk. AU - Jang, Ik Kyung. AU - Shin, Dong Ho. AU - Ko, Young Guk. AU - Choi, Donghoon. AU - Hong, Myeongki. AU - Cho, Yun Kyeong. AU - Nam, Chang Wook. AU - Hur, Seung Ho. AU - Choi, Jin Ho. AU - Song, Young Bin. AU - Hahn, Joo Yong. AU - Choi, Seung Hyuk. AU - Gwon, Hyeon Cheol. AU - Jang, Yangsoo. PY - 2012/4/1. Y1 - 2012/4/1. N2 - Background: Data on strut surface coverage of second-generation drug-eluting stents (DES) are limited. We investigated stent strut coverage of resolute zotarolimus-eluting stent (ZES-R) or everolimus-eluting stent (EES) at 9 months after implantation using optical coherence tomography (OCT). Methods: ComparisOn of neointimal coVerage betwEen zotaRolimus-eluting stent and everolimus-eluting stent using Optical Coherence Tomography (COVER OCT) is a prospective, randomized, ...
The present study is the first to demonstrate that a continuous supply of tissue kallikrein by way of gene transfer suppresses neointima formation in balloon-injured artery. Balloon angioplasty resulted in decreased endogenous rat tissue kallikrein expression. Expression of recombinant human tissue kallikrein at the injured site results in significant reduction of intima/media ratio and neointima formation, and time-dependent increases of cAMP and cGMP levels. Icatibant, a bradykinin B2 receptor antagonist, abolished both the protected effect of kallikrein on arterial thickening and the increases in cAMP and cGMP levels. Kallikrein gene transfer also suppresses the proliferation of VSMCs in vitro. These results suggest that inhibition of neointima formation in injured artery after kallikrein gene delivery is mediated by kinin with subsequent activation of second messengers such as cAMP and cGMP in blood vessels. These findings provide important insights into the role of the vascular ...
METHODS AND RESULTS: PI3K/p110α was inhibited by treatment with the small molecule inhibitor PIK75 or a specific siRNA. Arterial thrombosis, neointima formation, and re-endothelialization were studied in a murine carotid artery injury model. Proliferation and migration of human vascular smooth muscle cell (VSMC) and endothelial cell (EC) were assessed by cell number and Boyden chamber, respectively. Endothelial senescence was evaluated by the β-galactosidase assay, endothelial dysfunction by organ chambers for isometric tension. Arterial thrombus formation was delayed in mice treated with PIK75 when compared with controls. PIK75 impaired arterial expression and activity of tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1); in contrast, plasma clotting and platelet aggregation did not differ. In VSMC and EC, PIK75 inhibited expression and activity of TF and PAI-1. These effects occurred at the transcriptional level via the RhoA signalling cascade and the transcription factor ...
Mitoxantrone suppresses vascular smooth muscle cell (VSMC) proliferation and balloon injury-induced neointima formation: An in vitro and in vivo study
Here we provide the first evidence that 2-ME protects against injury-induced neointima formation in rats and arrests growth of human aortic SMCs via double blockade of the cell cycle. We demonstrate that 2-ME: (1) arrests proliferating SMCs in G0/G1 and G2/M-phases; (2) inhibits the signaling pathways ERK1/2 and Akt; (3) inhibits the expression and activation of key proteins responsible for the progression of cells into the DNA replicating phase (such as cyclin D1 expression and cdk4 activity associated with it and pRb phosphorylation); (4) upregulates the expression of the cdk inhibitor p27, suggesting that 2-ME can block HASMCs in G0/G1 phase via 2 different mechanisms; (5) inhibits cyclin B1 expression and cdk1 activity associated with it (essential for G2-to-M progression); (6) inhibits tubulin polymerization, a critical process in cell division; (7) induces COX-2 expression (known to mediate antiproliferative actions in SMCs); and (8) does not induce apoptosis, suggesting that the growth ...
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Peripheral Vascular Interventions: An Illustrated Manual by Juergen Schroeder English | 2013 | ISBN: 3131697512 | 240 pages | PDF | 6,4 MB Peripheral Vascular Interventions: An Illustrated M
BACKGROUND: Recent studies indicate that the smooth muscle-like cells contributing to neointimal hyperplasia after vascular injury derive from circulating precursor cells. Here, we define the time course of precursor cell influx, the roles of separat
Researchers at the University of Ulster, UK, have developed a 3D plasma coating technique to prevent stents from developing neointima, where thick muscle tissue grows over the surface, leading to the blood vessel narrowing again. Thin films of carbon,
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... the so-called neointima. Development of a neointima is variable but can at times be so severe as to re-occlude the vessel lumen ... Consequently, current research focuses on the reduction of neointima after stent placement. Substantial improvements have been ...
... mouse show reduced neointima formation. The association of ADAMTS7 with atherosclerosis suggests that inhibition of ADAMTS7 ... "ADAMTS-7 mediates vascular smooth muscle cell migration and neointima formation in balloon-injured rat arteries". Circulation ...
Minocycline inhibits smooth muscle cell proliferation, migration and neointima formation after arterial injury. J Cardiovasc ...
... expression in arterial wall after balloon angioplasty correlates with late stages of neointima formation and ... the exact role of T-cadherin in neointima formation and atherosclerosis development is poorly understood. LDL is not the only ...
August 2010). "Cellular mechanisms by which proinsulin C-peptide prevents insulin-induced neointima formation in human ...
"LincRNA-p21 regulates neointima formation, vascular smooth muscle cell proliferation, apoptosis, and atherosclerosis by ...
"Adenoviral expression of a urokinase receptor-targeted protease inhibitor inhibits neointima formation in murine and human ...
... Blocks Proliferation and Migration of Vascular Smooth Muscle Cells in Vitro and Reduces Neointima Formation in Vivo ...
... upregulated during neointima formation in a rat carotid endarterectomy model". Biochimica et Biophysica Acta. 1576 (1-2): 225- ...
Khachigian, L.M. et al (2002) c-Jun regulates vascular smooth muscle cell growth and neointima formation after arterial injury ...
... a paclitaxel coating limits the growth of neointima (scar tissue) within stents. Paclitaxel drug eluting coated stents for ...
... porous polyester stent reduces vein graft neointima formation, cholesterol concentration, and vascular cell adhesion molecule 1 ...
"Adenovirus-mediated gene transfer of human platelet-activating factor-acetylhydrolase prevents injury-induced neointima ...
The term neointima is used because the cells in the hyperplastic regions of the vascular wall have histological characteristics ...
... is overexpressed in vascular smooth muscle cells of atherosclerotic lesions and in the neointima of restenosis after ...
Functional neointima characterization of vascular prostheses in human. Ann Thorac Surg. 2004; 77: 864-8 Walles T, Giere B, ...
... can form as a result of vascular surgery such as angioplasty or stent placement. It is actually due to proliferation ... Neointima typically refers to scar tissue that forms within tubular anatomical structures such as blood vessels, as the intima ...
Along with neointima size, we will measure production of chemokines (IL-6, MCP-1, SDF-11, and KC), recruitment of bone marrow- ... The role of smooth muscle PPAR gamma in neointima formation Furgeson, Seth Bernat University of Colorado Denver, Aurora, CO, ... At multiple time points, neointima size will again be measured. All mice used in Aim 3B will have the R26R reporter allele in ... The role of smooth muscle PPAR gamma in neointima formation. Furgeson, Seth Bernat / University of Colorado Denver. $130,446. ...
Neointima can form as a result of vascular surgery such as angioplasty or stent placement. It is actually due to proliferation ... Neointima typically refers to scar tissue that forms within tubular anatomical structures such as blood vessels, as the intima ...
Medical definition of neointima: a new or thickened layer of arterial intima formed especially on a prosthesis or in ... Learn More about neointima. Share neointima Post the Definition of neointima to Facebook Share the Definition of neointima on ... Comments on neointima What made you want to look up neointima? Please tell us where you read or heard it (including the quote, ... Dictionary Entries near neointima. neo-Freudian neogenetic neohesperidin dihydrochalcone neointima neologism neomorph neomycin ...
Figure 2 : SRSF1 deficiency in VSMCs inhibits neointima formation.. From: SRSF1 promotes vascular smooth muscle cell ... neointima; M, media); n=9 per group. (e,f) Representative photomicrographs of immunohistochemical staining (scale bar, 25 μm) ( ... neointima/media ratio, media area and circumference of external elastic lamina (EEL) of carotid arteries from Srsf1−/− and WT ...
neointima definition: Noun (plural neointimas or neointimae) 1. (anatomy) A new layer of arterial intima, especially that ... neointima. Noun (plural neointimas or neointimae). *(anatomy) A new layer of arterial intima, especially that formed on a ... How would you define neointima? Add your definition here.. Please enable JavaScript to view the comments powered by Disqus.. ...
Abstract 14668: Epac1 Deficiency Inhibit Neointima Formation After Vascular Injuryin vivo. Yuko Kato, Utako Yokoyama, Satoshi ... Conclusion:These results suggest that Epac1 deficiency inhibit neointima formation after vascular injury in vivo. ... Abstract 14668: Epac1 Deficiency Inhibit Neointima Formation After Vascular Injuryin vivo ... Abstract 14668: Epac1 Deficiency Inhibit Neointima Formation After Vascular Injuryin vivo ...
C1-esterase inhibitor protects against neointima formation after arterial injury in atherosclerosis-prone mice. ... Search: C1[Title] AND esterase[Title] AND inhibitor[Title] AND protects[Title] AND against[Title] AND neointima[Title] AND ... C1[Title] AND esterase[Title] AND inhibitor[Title] AND protects[Title] AND against[Title] AND neointima[Title] AND formation[ ... Search: C1 esterase inhibitor protects against neointima formation aft.... *. Number of items displayed:. 5. 10. 15. 20. 50. ...
The apparent number of these receptors was fourfold higher in the neointima compared to that in the normal aortic wall. The ... Angiotensin-converting enzyme binding in the neointima was not different from that in the media of the uninjured aorta. Our ... Balloon angioplasty enhances the expression of angiotensin II AT1 receptors in neointima of rat aorta.. ... Balloon angioplasty enhances the expression of angiotensin II AT1 receptors in neointima of rat aorta.. ...
March 2018): Deletion of MFGE8 Inhibits Neointima Formation upon Arterial Damage. In: Thrombosis and Haemostasis, Vol. 118, No ...
Abstract 20944: Perivascular Progenitor Cells Contribute To Neointima Formation After Wire-induced Injury. Jan-Marcus Daniel, ... In conclusion, we provide evidence that BMPCs within the neointima rarely co-express markers for vascular cells and do not ... Most of the accumulating EGFP+-cells were identified as inflammatory cells (CD45, CD68), and their number in the neointima ... Abstract 20944: Perivascular Progenitor Cells Contribute To Neointima Formation After Wire-induced Injury ...
Whether AMPK alpha alters vascular neointima formation induced by vascular injury is unknown.Objective: The aim of this study ... Finally, neointima formation after mechanical arterial injury was increased in AMPK alpha 2(-/-) but not AMPK alpha 1(-/-) mice ... Objective: The aim of this study was to determine the roles of AMPK alpha in the development of vascular neointima hyperplasia ... Song, P., Wang, S., He, C., Wang, S., Liang, B., Viollet, B., & Zou, M-H. (2011). AMPK alpha 2 deletion exacerbates neointima ...
Arginase Promotes Neointima Formation in Rat Injured Carotid Arteries. Kelly J. Peyton, Diana Ensenat, Mohammed A. Azam, Amit N ... Arginase Promotes Neointima Formation in Rat Injured Carotid Arteries. Kelly J. Peyton, Diana Ensenat, Mohammed A. Azam, Amit N ... Arginase Promotes Neointima Formation in Rat Injured Carotid Arteries. Kelly J. Peyton, Diana Ensenat, Mohammed A. Azam, Amit N ...
When one considers, however, the percentage of neointima actually removed, even with the largest rotablator burrs, the commonly ... New recipes for in-stent restenosis: cut, grate, roast, or sandwich the neointima? ... New recipes for in-stent restenosis: cut, grate, roast, or sandwich the neointima? ... removal of neointima is the best method of treating in-stent restenosis but, in order for it to be practical and effective, new ...
Animals treated with empty gel exhibited a significant and concentric neointima. In contrast, a markedly diminished neointima ... Arginase Promotes Neointima Formation in Rat Injured Carotid Arteries. Kelly J. Peyton, Diana Ensenat, Mohammed A. Azam, Amit N ... Arginase Promotes Neointima Formation in Rat Injured Carotid Arteries. Kelly J. Peyton, Diana Ensenat, Mohammed A. Azam, Amit N ... Arginase Promotes Neointima Formation in Rat Injured Carotid Arteries. Kelly J. Peyton, Diana Ensenat, Mohammed A. Azam, Amit N ...
Finally, neointima formation in a model of rat carotid artery balloon injury was significantly attenuated after treatment with ... These data demonstrate that LXR ligands inhibit VSMC proliferation and neointima formation after balloon injury and suggest ... Liver X receptor agonists suppress vascular smooth muscle cell proliferation and inhibit neointima formation in balloon-injured ...
BuMA OCT Study(A Comparative Evaluation of the Extent of Neointima Formation at 3 Months After Implantation Using OCT). The ... The objective of this study is a comparative evaluation of BuMA stent and of EXCEL stent in terms of the extent of neointima ... BuMA OCT Study(A Comparative Evaluation of BuMA Stent and of EXCEL Stent in Terms of the Extent of Neointima Formation at 3 ... Neointima. Cardiovascular Diseases. Pathologic Processes. Chest Pain. Pain. Neurologic Manifestations. Nervous System Diseases ...
... mm2 and of the neointima 1.34 (0.08) mm2. The thickness of the neointima at each strut was 0.17 (0.01) mm. ... The quantity of neointima is directly proportional to the amount of injury inflicted upon the artery by the stent itself.1 That ... Gunn J, Arnold N, Chan KH, et al. Coronary artery stretch versus deep injury in the development of in-stent neointima. Heart ... We have shown that stent induced stretch of coronary arteries results in a neointima whose magnitude is directly related to a ...
Role of kinins and nitric oxide in the effects of ACE inhibition on neointima formation. Circ Res. 1993;72:1202-1210. ... Inhibition of neointima formation in rat carotid artery after adenovirus-mediated kallikrein gene delivery. A through D show ... Smooth-muscle-cell proliferation and differentiation in neointima formation and vascular restenosis. Clin Sci. 1994;87:467-479. ... The lumen, neointima, media areas were measured by use of the NIH Image 1.60 software package. ...
However, the role of IRF3 in vascular neo-intima formation is unknown. We evaluated the protective role of IRF3 against neo- ... Global knockout of IRF3 (IRF3-KO) led to accelerated neo-intima formation and proliferation of VSMCs, whereas the opposite was ... Vascular smooth muscle cell (VSMC) proliferation is central to the pathophysiology of neo-intima formation. Interferon ... IRF3 inhibits VSMC proliferation and neo-intima formation after vascular injury through PPARγ activation. ...
Neointima. Specific binding of [125I-Tyr0]CNP-(1-22) occurred throughout the neointima but tended to be most concentrated near ... Development of Neointima. The neointima developed as originally described27 for this preparation. Control arteries had no cells ... occurred in 7-day neointima, and 34±10/mm2 were present in neointima at 20 days (Fig 1⇓). ... NPR-C-like receptors also occur on the neointima. These findings are important because both NPR-B6 7 8 and NPR-C-like receptors ...
Characterization of the neointima revealed that WT (n=8) and Csrp2−/− (n=8) neointima had similar cell densities (19.6±0.5 and ... Increased Neointima Formation in Cysteine-Rich Protein 2-Deficient Mice in Response to Vascular Injury. Jiao Wei, Terri E. ... In Csrp2−/− mice (n=9) (Figure 6F), we observed 7.1±2.7% of BrdUrd incorporation in the neointima (P=0.63 versus WT) and 6.0± ... The cells observed in the neointima at the 4-day time point might reflect migrated rather than proliferating cells.6,7 En face ...
Core2 1-6-N-glucosaminyltransferase-I deficiency protects injured arteries from neointima formation in ApoE-deficient mice. - ... Arterial neointima induced by wire injury was smaller in C2GlcNAcT-I-deficient apoE(-/-) mice than in control apoE(-/-) mice (a ... Core2 1-6-N-glucosaminyltransferase-I deficiency protects injured arteries from neointima formation in ApoE-deficient mice.. ... C2GlcNAcT-I deficiency suppresses injury-induced arterial neointima formation, and this effect is attributable to decreased ...
We studied which of the events leading to neointima formation are involved in the effects of ACEI ... decrease neointima formation, and a kinin receptor antagonist partially reverses this inhibitory effect. ... 2) in the neointima, and this effect was abolished by cotreatment with icatibant (P < 0.05).ConclusionThe ACEI needs to be ... We studied which of the events leading to neointima formation are involved in the effects of ACEI and kinins.MethodsWe ...
2-Methoxyestradiol, an estradiol metabolite, inhibits neointima formation and smooth muscle cell growth via double blockade of ... Download PDF 2-Methoxyestradiol, an estradiol metabolite, inhibits neointima formation and smooth muscle cell growth via ... In rats, treatment with 2-ME abrogated injury-induced neointima formation; decreased proliferating SMCs; downregulated ... In rats, treatment with 2-ME abrogated injury-induced neointima formation; decreased proliferating SMCs; downregulated ...
Endovascular procedures cause transient endothelial injury but do not disrupt mature neointima in Drug Eluting Stents. ... Imaging of in-stent neointima at 28 days after stent placement did not lead to neointimal rupture. Guidewire, IVUS and OCT ... Endovascular procedures cause transient endothelial injury but do not disrupt mature neointima in Drug Eluting Stents. ...
Arterial thrombosis, neointima formation, and re-endothelialization were studied in a murine carotid artery injury model. ... Arterial thrombosis, neointima formation, and re-endothelialization were studied in a murine carotid artery injury model. ... Download PDF PI3K/p110α inhibition selectively interferes with arterial thrombosis and neointima formation, but not re- ... PI3K/p110α inhibition selectively interferes with arterial thrombosis and neointima formation, but not re-endothelialization: ...
MOBILIZATION OF ENDOTHELIAL PROGENITOR CELLS AND NEOINTIMA FORMATION AFTER IMPLANTATION OF EPC-CAPTURE STENTS IN NSTE-ACS (JACK ... MOBILIZATION OF ENDOTHELIAL PROGENITOR CELLS AND NEOINTIMA FORMATION AFTER IMPLANTATION OF EPC-CAPTURE STENTS IN NSTE-ACS (JACK ... MOBILIZATION OF ENDOTHELIAL PROGENITOR CELLS AND NEOINTIMA FORMATION AFTER IMPLANTATION OF EPC-CAPTURE STENTS IN NSTE-ACS (JACK ...
PAR-2 mediates increased inflammatory cell adhesion and neointima formation following vascular injury in the mouse ... Since adhesion of leukocytes is increased following vascular injury and is important in determining the extent of neointima ... protease activated receptor-2 (PAR-2), lymphocyte, vascular injury, adhesion, neointima, pharmacology, Therapeutics. ... PAR-2 mediates increased inflammatory cell adhesion and neointima formation following vascular injury in the mouse. ...
neointima, farnesyl transferase inhibitor, arteries, angioplasty, Pharmacy and materia medica, Cardiology and Cardiovascular ... Short-term local delivery of an inhibitor of ras farnesyltransferase prevents neointima formation in vivo after porcine ... it can inhibit neointima formation. Methods and Results- FPTIII (1 to 25 µmol/L) concentration-dependently reduced p21ras ... Application of 25 µmol/L FPTIII locally for 15 minutes to balloon-injured porcine coronary arteries in vivo prevented neointima ...
Short-term local delivery of an inhibitor of ras farnesyltransferase prevents neointima formation in vivo after porcine ... Application of 25 μmol/L FPTIII locally for 15 minutes to balloon-injured porcine coronary arteries in vivo prevented neointima ... Short-term local delivery of an inhibitor of ras farnesyltransferase prevents neointima formation in vivo after porcine ...
Poldip2 knockdown inhibits vascular smooth muscle proliferation and neointima formation by regulating the expression of PCNA ... p21 inhibits vascular smooth muscle cell proliferation and neointima formation in the rat carotid artery model of balloon ... p21 inhibits vascular smooth muscle cell proliferation and neointima formation in the rat carotid artery model of balloon ...
  • However, an absence of CRP2 enhanced VSMC migration and increased neointima formation following arterial injury. (ahajournals.org)
  • Stent implantation under low flow is associated with increased neointima formation. (uthscsa.edu)
  • Objective: The aim of this study was to determine the roles of AMPK alpha in the development of vascular neointima hyperplasia and to elucidate the underlying mechanisms. (rti.org)
  • CONCLUSIONS: NADPH oxidase is implicated in vascular remodelling and superoxide-stimulated cell proliferation in the neointima contributes to intimal hyperplasia in this collar model. (edu.au)
  • The result of these vascular events is intimal hyperplasia, whereby vascular smooth muscle cells (VSMCs) migrate from the media to the intima, proliferate, and consequently, form the neointima. (aspetjournals.org)
  • CD9 is upregulated in senescent endothelial cells, neointima hyperplasia, and atherosclerotic plaques. (nature.com)
  • Neointima hyperplasia was minimal in the single-PED-group animals. (ajnr.org)
  • 15 We observed a strong reduction in neointima hyperplasia and media thickening in hepatocyte-specific, gp130-deficient mice, which was associated with reduced local vascular inflammation, as well as reduced SMC content and proliferation in the vessel wall. (ahajournals.org)
  • Liver X receptor agonists suppress vascular smooth muscle cell proliferation and inhibit neointima formation in balloon-injured rat carotid arteries. (nih.gov)
  • 5 Specific Ang II receptor antagonists can also partially inhibit neointima formation, which suggests that the inhibition of neointima formation by ACE inhibitors is, in part, because of a decreased level of Ang II. (ahajournals.org)
  • Our aim was to demonstrate in biochemical studies that farnesyl protein transferase inhibitor III (FPTIII) is an inhibitor of p21ras processing and that when it is given locally in vivo at the site of coronary balloon injury in a porcine model, it can inhibit neointima formation. (strath.ac.uk)
  • Neointima can form as a result of vascular surgery such as angioplasty or stent placement. (wikipedia.org)
  • Balloon angioplasty enhances the expression of angiotensin II AT1 receptors in neointima of rat aorta. (jci.org)
  • The lumen enlargement after balloon angioplasty is the combined effect of further stent expansion and extrusion-axial redistribution of the neointima. (bmj.com)
  • Adenovirus-mediated over-expression of the cyclin/cyclin-dependent kinase inhibitor, p21 inhibits vascular smooth muscle cell proliferation and neointima formation in the rat carotid artery model of balloon angioplasty. (semanticscholar.org)
  • Neointima formation occurs frequently after angioplasty and causes significant morbidity;vascular smooth muscle cells (SMCs) are key cells during neointima formation. (grantome.com)
  • Conclusion: With some evidence of dose-dependence, tissue plasminogen activator enhances neointima formation after angioplasty in a rabbit model. (elsevier.com)
  • We have studied the effects of autologous platelets, electroloaded with the stable prostacyclin analogue, iloprost on platelet deposition and neointima formation in a pig carotid angioplasty model. (ox.ac.uk)
  • Acute platelet deposition was measured using 111-Indium, and neointima formation at 21 days post angioplasty was assessed by morphometric analysis. (ox.ac.uk)
  • Maladaptive remodelling of the arterial wall after mechanical injury (e. g. angioplasty) is characterised by inflammation, neointima formation and media hypertrophy, resulting in narrowing of the affected artery. (nih.gov)
  • Methods and Results- Balloon injury of rat carotid arteries resulted in a sustained increase in arginase activity in the vessel wall and the induction of arginase I protein in both the media and neointima of injured vessels. (ahajournals.org)
  • Objective In balloon-injured rat carotid arteries, angiotensin-converting enzyme inhibitors (ACEI) decrease neointima formation, and a kinin receptor antagonist partially reverses this inhibitory effect. (ovid.com)
  • Local delivery of platelets with encapsulated iloprost to balloon injured pig carotid arteries: effect on platelet deposition and neointima formation. (ox.ac.uk)
  • Western blotting analysis revealed that both cathepsin S and K protein levels also increased in the carotid arteries during neointima formation, coinciding with an increase elastolytic activity assayed using Elastin-Congo red, whereas, no significant change in the expressions of cystatin C mRNA and protein was observed during follow-up periods after injury. (elsevier.com)
  • Endothelial cell repopulation after stenting determines in-stent neointima formation: effects of bare-metal vs. drug-eluting stents and genetic endothelial cell modification. (ox.ac.uk)
  • CONCLUSION: Drug-eluting stents reduce not only neointima formation but also endothelial cell repopulation, independent of strut coverage. (ox.ac.uk)
  • Bone marrow-derived progenitor cells (BMPCs) as well as perivascular progenitor cells have been implicated to differentiate into vascular cells during neointima formation. (ahajournals.org)
  • We also plan to study the role of PPAR3 activation specifically in smooth muscle cells during neointima formation. (grantome.com)
  • Results: Both rate and degree of neointima formation increase dramatically with overexpression (250%-461% relative to controls at 7 and 28 days). (elsevier.com)
  • Systemic infusion, although significant, did not attain the degree of neointima formation present with overexpression. (elsevier.com)
  • Common hepatic lipase gene promoter variant predicts the degree of neointima formation after carotid endarterectomy: impact of plaque composition a. (cdc.gov)
  • The objective of this study is a comparative evaluation of BuMA stent and of EXCEL stent in terms of the extent of neointima formation at 3 months after implantation using OCT. (clinicaltrials.gov)
  • Since adhesion of leukocytes is increased following vascular injury and is important in determining the extent of neointima formation, we hypothesised that mice lacking PAR-2 may have reduced neointima formation following vascular injury. (strath.ac.uk)
  • C1-esterase inhibitor protects against neointima formation after arterial injury in atherosclerosis-prone mice. (nih.gov)
  • Finally, neointima formation after mechanical arterial injury was increased in AMPK alpha 2(-/-) but not AMPK alpha 1(-/-) mice. (rti.org)
  • Core2 1-6-N-glucosaminyltransferase-I deficiency protects injured arteries from neointima formation in ApoE-deficient mice. (curehunter.com)
  • Arterial neointima induced by wire injury was smaller in C2GlcNAcT-I-deficient apoE (-/-) mice than in control apoE (-/-) mice (a 79% reduction in size). (curehunter.com)
  • PF4 deficiency accelerated endothelial regeneration and protected mice from neointima formation after arterial injury. (curehunter.com)
  • Our data show that PAR-2 modulates inflammatory cell adhesion when stimulated and in mice lacking the PAR-2 receptor, adhesion to injured vessels is reduced with a consequent reduction in neointima formation. (strath.ac.uk)
  • Histological examination revealed that the neointima is markedly thickened in A2bAR KO mice compared with WT mice. (pnas.org)
  • METHODS AND RESULTS: Endothelial cell repopulation was assessed en face in stented arteries in ApoE(-/-) mice with endothelial-specific LacZ expression. (ox.ac.uk)
  • GCH-Tg ApoE(-/-) mice had less neointima formation compared with ApoE(-/-) littermates (0.52 ± 0.08 vs. 0.26 ± 0.09 mm(2), P = 0.039). (ox.ac.uk)
  • In contrast to paclitaxel-eluting stents, reduced neointima formation in GCH-Tg mice was accompanied by increased endothelial cell coverage (156 ± 17 vs. 209 ± 23 nuclei/mm(2), P = 0.043). (ox.ac.uk)
  • Neointima formation was investigated after vascular injury in FSAP -/- mice. (cdc.gov)
  • Objectives To determine whether neointima formation after vascular injury is increased in FSAP -/- mice. (cdc.gov)
  • Irisin treatment (0.5 μg/g body weight/day) significantly reduced the severity of aortic atherosclerosis in apolipoprotein E-deficient mice fed on a high-cholesterol diet and suppressed carotid neointima formation in a carotid partial ligation model. (plos.org)
  • The aims of this work were to determine if aPLs directly promote medial hypertrophy or neointima formation in mice and to identify the underlying mechanisms. (elsevier.com)
  • Methods and Results-Medial hypertrophy and neointima formation invoked by carotid artery endothelial denudation were evaluated in mice administered normal human IgG or aPLs. (elsevier.com)
  • Conclusions-APLs blunt endothelial repair, and there is related aPL-induced exaggeration in neointima formation after endothelial injury in mice. (elsevier.com)
  • In conclusion, we provide evidence that BMPCs within the neointima rarely co-express markers for vascular cells and do not contribute to the neointimal cellular mass beyond the inflammatory response. (ahajournals.org)
  • Furthermore, local perivascular application of the potent and selective arginase inhibitors S -(2-boronoethyl)- l -cysteine (BEC) or N G -hydroxy-nor- l -arginine (L-OHNA) immediately after injury markedly attenuated medial and neointimal DNA synthesis and neointima formation. (ahajournals.org)
  • For each section (n = 99), with its associated neointimal and luminal areas, we measured the number of struts, percentage metal coverage of the arterial wall, stent major and minor axes, stent oblateness, and areas of the lumen and the neointima. (bmj.com)
  • Imaging of in-stent neointima at 28 days after stent placement did not lead to neointimal rupture. (eur.nl)
  • Animals treated with cilazapril (10 mg/kg/day) had markedly reduced neointima formation, but in animals receiving infusion of Ang II, treatment with cilazapril did not suppress development of neointimal lesions. (elsevier.com)
  • In contrast, selective targeting of endothelial cell function is sufficient to improve endothelial cell repopulation and reduce neointima formation. (ox.ac.uk)
  • Our hypothesis is that PPAR3 activation specifically in smooth muscle cells (SMC) will reduce neointima formation by decreasing resident SMC migration and proliferation as well as SMC-derived chemokine production and subsequent recruitment of bone marrow-derived cells. (grantome.com)
  • Factor VII-activating protease deficiency promotes neointima formation by enhancing leukocyte accumulation. (cdc.gov)
  • Targeting endothelial cell function is a rational therapeutic strategy to improve vascular healing and decrease neointima formation after stenting. (ox.ac.uk)
  • However, the exact mechanism and mediators responsible for VSMC activation and neointima formation after injury of the vessel wall remain elusive. (ahajournals.org)
  • These data demonstrate that LXR ligands inhibit VSMC proliferation and neointima formation after balloon injury and suggest that LXR ligands may constitute a novel therapy for proliferative vascular diseases. (nih.gov)
  • CONCLUSIONS: We conclude that TRAIL induction involves FGF-2, Sp1-phosphorylation and NFκB and that TRAIL promotes VSMC proliferation and neointima formation after arterial injury. (sahmriresearch.org)
  • Experimental injury of the rat aorta causes rapid migration of medial smooth muscle cells and their proliferation resulting in the formation of neointima. (jci.org)
  • We have examined, using quantitative autoradiography, the expression of angiotensin II receptor subtypes AT1 and AT2, and angiotensin-converting enzyme, in the neointima formed in the rat thoracic aorta 15 d after balloon-catheter injury. (jci.org)
  • Whether AMPK alpha alters vascular neointima formation induced by vascular injury is unknown. (rti.org)
  • This study investigated the impact of arginase on cell cycle progression and neointima formation after experimental arterial injury. (ahajournals.org)
  • Finally, neointima formation in a model of rat carotid artery balloon injury was significantly attenuated after treatment with the LXR ligand T1317 compared with vehicle-treated animals. (nih.gov)
  • The quantity of neointima is directly proportional to the amount of injury inflicted upon the artery by the stent itself. (bmj.com)
  • We have previously shown that stretch is ubiquitous after stenting and, even in the absence of deep injury, is an important mediator of neointima formation. (bmj.com)
  • Therefore, in this study, we aimed to examine the contribution of a wide panel of parameters of stent geometry to the development of neointima in stent sections that displayed stretch but not deep injury. (bmj.com)
  • 4 Angiotensin-converting enzyme (ACE) inhibitor suppresses neointima formation after endothelial injury in rat carotid artery and abdominal aorta. (ahajournals.org)
  • Thus, whereas levels of NPR-B did not change significantly after arterial injury and NPR-A was not detected, NPR-C-like receptors were unregulated as mitosis declined in the media and as a prominent neointima formed. (ahajournals.org)
  • C2GlcNAcT-I deficiency suppresses injury-induced arterial neointima formation , and this effect is attributable to decreased leukocyte recruitment to injured vascular walls and increased endothelial regeneration. (curehunter.com)
  • Methods We administered 5 mg/kg per day ramipril, either alone or combined with the kinin receptor antagonist icatibant (Hoe 140), on the days each wave occurred and studied the effects on neointima formation 14 days after balloon injury. (ovid.com)
  • Ramipril alone or combined with icatibant had no effect on neointima formation when administered from 2 days before to 3 or 5 days after balloon injury. (ovid.com)
  • Here we studied the intracellular mechanisms by which 2-ME inhibits SMC growth and whether 2-ME prevents injury-induced neointima formation. (uzh.ch)
  • Arterial thrombosis, neointima formation, and re-endothelialization were studied in a murine carotid artery injury model. (uzh.ch)
  • In line with this observation, treatment with PIK75 selectively inhibited neointima formation without affecting re-endothelialization following vascular injury. (uzh.ch)
  • CONCLUSION: Following vascular injury, PI3K/p110α inhibition selectively interferes with arterial thrombosis and neointima formation, but not re-endothelialization. (uzh.ch)
  • In Aim Three, we will determine which agent can reduce neointima size the greatest after wire injury. (grantome.com)
  • Angiotensin converting enzyme inhibition markedly suppresses neointima formation in response to balloon catheter-induced vascular injury of the rat carotid artery. (elsevier.com)
  • Animals that received continuous infusion of Ang II (0.3 μg/min/rat) were found to have significantly greater neointima formation in response to balloon injury than controls. (elsevier.com)
  • These data support the conclusions that converting enzyme inhibition prevents neointima formation after vascular injury through inhibition of Ang II generation. (elsevier.com)
  • This concept may have clinical ramifications given that factors which enhance interstitial flow (i.e., chemical or mechanical injury to the endothelium and inflammation and hypertension induced enhancement of vascular permeability) are associated with vessel remodeling and neointima formation. (semanticscholar.org)
  • MK2-deficiency (ldlr-/-/mk2-/-) nearly completely prevented neointima formation, media hypertrophy, and lumen loss after injury. (nih.gov)
  • Accumulating evidence shows that inhibition of the vascular renin-angiotensin system results in suppression of injury-elicited neointima formation. (nii.ac.jp)
  • We attempted to determine whether or not combined treatment with an angiotensin II type 1 receptor blocker (ARB) and angiotensin converting enzyme inhibitor (ACEI) has an additive inhibitory effect on balloon-injury-elicited neointima formation in the carotid artery. (nii.ac.jp)
  • The glucose transporter isoform, GLUT1, was significantly increased in the neointima after balloon injury. (diabetesjournals.org)
  • Extracellular matrix remodeling after proatherosclerotic injury involves an increase in hyaluronan (HA) that is coupled with vascular smooth muscle cell (SMC) migration, proliferation, and with neointima formation. (biomedsearch.com)
  • Progressive atherosclerosis within the neointima is an another possible cause of LST, but this phenomenon has seldom been reported in DES. (bvsalud.org)
  • Although multiple factors contributing to late stent failure have been proposed, de novo development of atherosclerosis within the neointima has been identified as a major cause [ 5 , 6 ]. (hindawi.com)
  • Interestingly, an in vivo model of smooth muscle cell proliferation revealed that an A2 receptor agonist, 2-octynyladenosine, inhibited neointima formation ( 8 ). (pnas.org)
  • Figure 2: SRSF1 deficiency in VSMCs inhibits neointima formation. (nature.com)
  • The LIPC promoter -514 C-T polymorphism is associated with a significantly reduced development of neointima after surgery. (cdc.gov)
  • A2bAR Deficiency Enhances Postinjury Neointima Formation in the Vasculature. (pnas.org)
  • Further experiments showed that aPL antagonism of endothelial migration and repair is mediated by antibody recognition of β2-glycoprotein I, apolipoprotein E receptor 2, and a decline in bioavailable NO. Consistent with these mechanisms, the adverse impacts of aPLs on reendothelialization and neointima formation were fully prevented by the NO donor molsidomine. (elsevier.com)
  • 1-3 Neointima formation is one of the hallmarks of the remodeling process and involves cellular as well as structural changes of the vascular wall, 4 which are driven by local infiltration of inflammatory cells 5 and by migration and proliferation of resident medial smooth muscle cells (SMCs). (ahajournals.org)
  • We hypothesized that the differential enhancement of glucose metabolism in the neointima contributed to formation of lesions by increasing the resistance of VSMCs to apoptosis. (diabetesjournals.org)
  • C1 esterase inhibitor protects against neointima formation aft. (nih.gov)
  • We have now examined the action of the NADPH oxidase inhibitor apocynin, given via the adventitia, on the neointima formation and endothelial function in this model. (edu.au)
  • Each independent parameter (stent geometry) was tested for significance against each dependent parameter (lumen and neointima areas and thicknesses) to yield a list of stent geometry parameters that correlated with arterial morphometry. (bmj.com)
  • One of the drawbacks of vascular stents is the potential for restenosis via the development of a thick smooth muscle tissue inside the lumen, the so-called neointima. (wikipedia.org)
  • Development of a neointima is variable but can at times be so severe as to re-occlude the vessel lumen (restenosis), especially in the case of smaller diameter vessels, which often results in reintervention. (wikipedia.org)
  • FPTIII also prevented p42/p44 MAPK activation and DNA synthesis in response to platelet-derived growth factor in these cells at a concentration of 25 µmol/L. Application of 25 µmol/L FPTIII locally for 15 minutes to balloon-injured porcine coronary arteries in vivo prevented neointima formation assessed at 4 weeks, reduced proteoglycan deposition, and inhibited adventitial hypertrophy. (strath.ac.uk)
  • FPTIII also prevented p42/p44 MAPK activation and DNA synthesis in response to platelet-derived growth factor in these cells at a concentration of 25 μmol/L. Application of 25 μmol/L FPTIII locally for 15 minutes to balloon-injured porcine coronary arteries in vivo prevented neointima formation assessed at 4 weeks, reduced proteoglycan deposition, and inhibited adventitial hypertrophy. (gla.ac.uk)
  • While aPLs had no effect on medial hypertrophy, they caused exaggerated neointima development. (elsevier.com)
  • Example for neointima formation in a female rabbit aortic section after endothelial balloon denudation and 21 days of cultivation in medium containing 1 % isopropanol and 1 % DMSO. (biomedcentral.com)
  • We use either local adenoviral-mediated overexpression of tPA or systemic infusion of recombinant tPA combined with mechanical overdilation of rabbit common femoral arteries to evaluate the impact of tPA on neointima formation. (elsevier.com)
  • Curcumin significantly attenuates carotid artery neointima formation. (greenmedinfo.com)
  • In addition, apocynin significantly reduced neointima formation and proliferation of cells in both the neointima and adventitia. (edu.au)
  • The full-dose combination lowered blood pressure and suppressed neointima formation significantly compared with the levels in the groups treated with either ACEI or ARB alone. (nii.ac.jp)
  • Paclitaxel-eluting stents reduced neointima formation (0.423 ± 0.065 vs. 0.240 ± 0.040 mm(2), P = 0.038), but decreased endothelial cell repopulation (238 ± 17 vs. 154 ± 22 nuclei/mm(2), P = 0.018), despite complete strut coverage. (ox.ac.uk)
  • Consequently, current research focuses on the reduction of neointima after stent placement. (wikipedia.org)
  • The low-dose combination without blood pressure reduction also inhibited neointima formation to a similar extent as the full-dose combination. (nii.ac.jp)
  • Restenosis is caused by growth of a neointima, comprised of smooth muscle cells and intercellular matrix. (bmj.com)
  • Vascular smooth muscle cells are stained in the medial tissue and in the neointima. (biomedcentral.com)
  • Severe medial tear was associated with exuberant neointima. (medscape.com)
  • Neointima, which became evident 5 to 7 days after arterial damage, expressed NPR-C-like sites and no detectable NPR-B-like binding. (ahajournals.org)
  • We studied which of the events leading to neointima formation are involved in the effects of ACEI and kinins. (ovid.com)
  • In addition, ACEI, through kinins, affect a process that increases the density of the cells in the neointima, perhaps by decreasing extracellular matrix deposition. (ovid.com)
  • Both ARB and ACEI inhibited neointima formation without any blood pressure changes. (nii.ac.jp)
  • The increase in local kinin accumulation may also be involved in the inhibition of neointima formation because icatibant, a bradykinin B 2 receptor antagonist, can partially block the protective effect of ACE inhibitors. (ahajournals.org)
  • Neointima typically refers to scar tissue that forms within tubular anatomical structures such as blood vessels, as the intima is the innermost lining of these structures. (wikipedia.org)
  • Enhanced interstitial flow as a contributing factor in neointima formation: (shear) stressing vascular wall cell types other than the endothelium. (semanticscholar.org)
  • The capabilities of OCT are well suited for the identification of calcified plaque and neointima formation after stent implantation. (springer.com)
  • 2 ) in the neointima, and this effect was abolished by cotreatment with icatibant ( P (ovid.com)
  • Partial neointima covered the ostia of the branch vessels, but demonstrable patent lumens at the ostia in all cases were present. (ajnr.org)