Angiopoietin-2
Angiopoietin-1
Receptor, TIE-2
Angiopoietins
Receptor, TIE-1
Receptors, TIE
Angiogenesis Inducing Agents
Vascular Endothelial Growth Factor A
Neovascularization, Physiologic
Endothelial Cells
Neovascularization, Pathologic
Vascular Endothelial Growth Factors
Mycoplasma pulmonis
Angiogenic Proteins
Endothelial Growth Factors
Receptor Protein-Tyrosine Kinases
Lymphokines
Blood Vessels
Vascular Endothelial Growth Factor Receptor-2
Pericytes
Retinal Neovascularization
Endothelium, Vascular
Vascular Endothelial Growth Factor Receptor-1
Intercellular Signaling Peptides and Proteins
Cells, Cultured
Angiogenesis Inhibitors
RNA, Messenger
Signal Transduction
Receptors, Vascular Endothelial Growth Factor
In Situ Hybridization
Retinal Perforations
Immunohistochemistry
Capillary Permeability
Reverse Transcriptase Polymerase Chain Reaction
Fovea Centralis
Proteins
Diabetic Retinopathy
Up-Regulation
Receptors, Growth Factor
Umbilical Veins
Vitrectomy
Gene Expression Regulation
Vitreous Body
Proto-Oncogene Proteins
Blotting, Western
Macular Edema
Enzyme-Linked Immunosorbent Assay
Neoplasm Proteins
Disease Models, Animal
Cell Movement
Ischemia
Apoptosis
Gene Expression
Mice, Transgenic
Fibroblast Growth Factor 2
Transfection
Phosphorylation
Biological Markers
Cell Survival
Gene Expression Profiling
Mice, Knockout
Dose-Response Relationship, Drug
Pregnancy
Rats, Sprague-Dawley
Molecular cloning and characterization of a novel angiopoietin family protein, angiopoietin-3. (1/540)
Using homology-based PCR, we have isolated cDNA encoding a novel member (491 amino acids) of the angiopoietin (Ang) family from human adult heart cDNA and have designated it angiopoietin-3 (Ang3). The NH2-terminal and COOH-terminal portions of Ang-3 contain the characteristic coiled-coil domain and fibrinogen-like domain that are conserved in other known Angs. Ang3 has a highly hydrophobic region at the N-terminus (approximately 21 amino acids) that is typical of a signal sequence for protein secretion. Ang3 mRNA is most abundant in adrenal gland, placenta, thyroid gland, heart and small intestine in human adult tissues. Additionally, Ang3 is a secretory protein, but is not a mitogen in endothelial cells. (+info)Hypoxia and vascular endothelial growth factor selectively up-regulate angiopoietin-2 in bovine microvascular endothelial cells. (2/540)
Recent studies have shown that the angiopoietin-Tie2 system is a predominant regulator of vascular integrity. In this study, we investigated the effect of two known angiogenic stimuli, hypoxia and vascular endothelial growth factor (VEGF), on these molecules. VEGF induced both a time- and concentration-dependent increase in angiopoietin-2 (Ang2) mRNA expression in bovine microvascular endothelial cells. This up-regulation was derived primarily from an increased transcription rate as evidenced by nuclear run-on assay and mRNA decay study. The increased Ang2 expression upon VEGF treatment was almost totally abolished by inhibition of tyrosine kinase or mitogen-activated protein kinase and partially by suppression of protein kinase C. Hypoxia also directly increased Ang2 mRNA expression. In contrast, Ang1 and Tie2 responded to neither of these stimuli. The enhanced Ang2 expression following VEGF stimulation and hypoxia was accompanied by de novo protein synthesis as detected by immunoprecipitation. In a mouse model of ischemia-induced retinal neovascularization, Ang2 mRNA was up-regulated in the ischemic inner retinal layer, and remarkable expression was observed in neovascular vessels. These data suggest that both hypoxia- and VEGF-induced neovascularization might be facilitated by selective induction of Ang2, which deteriorates the integrity of preexisting vasculature. (+info)Vessel cooption, regression, and growth in tumors mediated by angiopoietins and VEGF. (3/540)
In contrast with the prevailing view that most tumors and metastases begin as avascular masses, evidence is presented here that a subset of tumors instead initially grows by coopting existing host vessels. This coopted host vasculature does not immediately undergo angiogenesis to support the tumor but instead regresses, leading to a secondarily avascular tumor and massive tumor cell loss. Ultimately, however, the remaining tumor is rescued by robust angiogenesis at the tumor margin. The expression patterns of the angiogenic antagonist angiopoietin-2 and of pro-angiogenic vascular endothelial growth factor (VEGF) suggest that these proteins may be critical regulators of this balance between vascular regression and growth. (+info)Expressions of angiopoietins and Tie2 in human choroidal neovascular membranes. (4/540)
PURPOSE: To elucidate the potential role of angiopoietins and the Tie2 system in choroidal neovascularization. METHODS: Surgically excised choroidal neovascular membranes (CNVMs) were obtained at vitrectomy from five eyes with age-related macular degeneration, three eyes with idiopathic neovascular maculopathy, and two eyes had degenerative myopia and two eyes had angioid streaks. Light microscopic immunohistochemistry was performed to detect cytokines such as vascular endothelial growth factor (VEGF), Ang1, and Ang2 and cellular components such as retinal pigment epithelial (RPE) cells, macrophages, and endothelial cells. Immunofluorescent double staining using confocal microscopy was performed to identify the cell types that secrete specific cytokines. RESULTS: Ang1 and Ang2 were positive in all surgically excised CNVMs, regardless of the primary disease. Double staining revealed that many of the cytokeratin, CD68 and factor VIII positive cells also had Ang1 and Ang2 immunoreactivities. In contrast to Ang1, Ang2 immunoreactivity tends to be higher in the highly vascularized regions of many CNVMs, and the localization was very similar to that of VEGF staining. Almost all vascular structures had prominent immunoreactivity for Tie2, which was confirmed by double staining for Tie2 and factor VIII. Tie2 immunoreactivity was also observed in the RPE monolayer and in pigmented, polygonal, and fibroblast-like cells in the stroma. CONCLUSIONS: Present findings that Ang2 and VEGF are co-upregulated and that Tie2 is expressed in a variety of cell types in CNVMs further support a crucial role of the interaction between VEGF and Ang2 in pathologic angiogenesis of CNVM formation. (+info)Expression of angiopoietin-1, angiopoietin-2, and the Tie-2 receptor tyrosine kinase during mouse kidney maturation. (5/540)
The Tie-2 receptor tyrosine kinase transduces embryonic endothelial differentiation, with Angiopoietin-1 (Ang-1) acting as a stimulatory ligand and Ang-2 postulated to be a naturally occurring inhibitor. Expression of these genes was sought during mouse kidney maturation from the onset of glomerulogenesis (embryonic day 14 [E14]) to the end of nephron formation (2 wk postnatal [P2]), and during medullary maturation into adulthood (P8). Using Northern and slot blotting of RNA extracted from whole organs, these three genes were expressed throughout the experimental period with peak levels at P2 to P3. By in situ hybridization analysis at E18, P1, and P3, Ang-1 mRNA was found to localize to condensing renal mesenchymal cells, proximal tubules, and glomeruli in addition to maturing tubules of the outer medulla. In contrast, Ang-2 transcripts were more spatially restricted, being detected only in differentiating outer medullary tubules and the vasa recta bundle area. Using in situ hybridization and immunohistochemistry, Tie-2 was detected in capillaries of the nephrogenic cortex, glomerular tufts, cortical interstitium, and medulla including vessels in the vasa recta. Using Western blotting of protein extracted from whole organs, Tie-2 protein was detected between E14 and P8 with tyrosine phosphorylated Tie-2 evident from E18. These data are consistent with the hypothesis that Tie-2 has roles in maturation of both glomeruli and vasa rectae. (+info)New model of tumor angiogenesis: dynamic balance between vessel regression and growth mediated by angiopoietins and VEGF. (6/540)
Our analyses in several different tumor settings challenge the prevailing view that malignancies and metastases generally initiate as avascular masses that only belatedly induce vascular support. Instead, we find that malignant cells rapidly co-opt existing host vessels to form an initially well-vascularized tumor mass. Paradoxically, the co-opted vasculature does not undergo angiogenesis to support the growing tumor, but instead regresses (perhaps as part of a normal host defense mechanism) via a process that involves disruption of endothelial cell/smooth muscle cell interactions and endothelial cell apoptosis. This vessel regression in turn results in necrosis within the central part of the tumor. However, robust angiogenesis is initiated at the tumor margin, rescuing the surviving tumor and supporting further growth. The expression patterns of Angiopoietin-2 (the natural antagonist for the angiogenic Tie2 receptor) and vascular endothelial growth factor (VEGF) strongly implicate these factors in the above processes. Angiopoietin-2 is highly induced in co-opted vessels, prior to VEGF induction in the adjacent tumor cells, providing perhaps the earliest marker of tumor vasculature and apparently marking the co-opted vessels for regression. Subsequently, VEGF upregulation coincident with Angiopoietin-2 expression at the tumor periphery is associated with robust angiogenesis. Thus, in tumors, Angiopoietin-2 and VEGF seem to reprise the roles they play during vascular remodeling in normal tissues, acting to regulate the previously underappreciated balance between vascular regression and growth. (+info)Angiopoietin-1 and -2 coiled coil domains mediate distinct homo-oligomerization patterns, but fibrinogen-like domains mediate ligand activity. (7/540)
Activity of endothelial Tie2 receptor tyrosine kinase is modulated by two naturally occurring, secreted ligands, angiopoietin-1 and -2, which have opposing effects on its phosphorylation. Receptor tyrosine kinase activation requires receptor dimerization/multimerization, which, for many receptors, is mediated by homo-oligomeric ligands binding to and bridging receptor molecules. We show here that angiopoietin-1 and -2 form distinct arrays of disulfide-linked homo-oligomeric complexes. Their mobilities on nonreducing gels suggest that angiopoietin-2 exists predominantly as a homodimer but also forms higher order multimers. In contrast, angiopoietin-1 forms some homotrimers, but predominantly exists in higher order multimers. These two structurally related, 60% homologous ligands are predominantly composed of an amino-terminal coiled coil domain and a carboxyl-terminal fibrinogen-like domain. We show that their distinct oligomerization patterns are determined by their coiled coil domains and, furthermore, that their coiled coil domains, but not their fibrinogen-like domains, are sufficient to mediate formation of disulfide-linked homo-oligomers. In contrast, the differential effects of these ligands on endothelial Tie2 phosphorylation is mediated by their fibrinogen-like domains. We conclude from these studies that the coiled coil and fibrinogen-like domains of the angiopoietins have distinct functions with the coiled coil domain mediating ligand homo-oligomerization and the fibrinogen-like domain mediating ligand activity. (+info)Vascular endothelial growth factor (VEGF) and angiopoietin regulation by gonadotrophin and steroids in macaque granulosa cells during the peri-ovulatory interval. (8/540)
The role of endothelial cell-specific growth factors in the vascularization of the primate peri-ovulatory follicle was examined. Experiments were designed firstly to detect expression of vascular endothelial growth factor (VEGF), angiopoietin-1 (Ang-1) and angiopoietin-2 (Ang-2) in granulosa cells and secondly, to determine whether gonadotrophins and/or steroids regulate their expression during the peri-ovulatory interval. Granulosa cells and follicular fluid were collected from rhesus macaques undergoing ovarian stimulation before (0 h), 12, or 36 h after a bolus of ovulatory human chorionic gonadotrophin (HCG), with or without steroid ablation and progestin replacement. VEGF, Ang-1 and Ang-2 mRNA were all detected prior to the ovulatory stimulus. Whereas follicular fluid VEGF concentrations increased 6-fold (P < 0.05) between 0 and 12 h, VEGF mRNA values were unchanged and were unaffected by steroid ablation. Ang-1 mRNA decreased from 0 to 12 h (P < 0.05), followed by a 30-fold increase (P < 0.05) at 36 h, while Ang-2 mRNA values were unchanged between 0, 12 and 36 h. Steroid ablation decreased (P < 0.05) Ang-1 mRNA at 36 h, and Ang-2 mRNA at 12 h, while only Ang-1 was restored by progestin replacement. These data suggest a dynamic expression of vascular-specific growth factors in a gonadotrophin-dependent, steroid-independent (VEGF) or steroid-dependent (Ang-1) manner in granulosa cells of peri-ovulatory follicles of primates. (+info)Pathologic neovascularization can be seen in a variety of conditions, including cancer, diabetic retinopathy, and age-related macular degeneration. In cancer, for example, the formation of new blood vessels can help the tumor grow and spread to other parts of the body. In diabetic retinopathy, the growth of new blood vessels in the retina can cause vision loss and other complications.
There are several different types of pathologic neovascularization, including:
* Angiosarcoma: a type of cancer that arises from the cells lining blood vessels
* Hemangiomas: benign tumors that are composed of blood vessels
* Cavernous malformations: abnormal collections of blood vessels in the brain or other parts of the body
* Pyogenic granulomas: inflammatory lesions that can form in response to trauma or infection.
The diagnosis of pathologic neovascularization is typically made through a combination of physical examination, imaging studies (such as ultrasound, CT scans, or MRI), and biopsy. Treatment options vary depending on the underlying cause of the condition, but may include medications, surgery, or radiation therapy.
In summary, pathologic neovascularization is a process that occurs in response to injury or disease, and it can lead to serious complications. It is important for healthcare professionals to be aware of this condition and its various forms in order to provide appropriate diagnosis and treatment.
The growth of new blood vessels in the retina is a natural response to hypoxia (lack of oxygen) and inflammation caused by these diseases. However, these new blood vessels are fragile and can cause damage to the retina, leading to vision loss. In some cases, RNV can also lead to vitreous hemorrhage, retinal detachment, or glaucoma, which can further exacerbate vision loss.
The diagnosis of RNV is typically made through a comprehensive eye exam, including a visual acuity test, dilated eye exam, and imaging tests such as fluorescein angiography or optical coherence tomography (OCT). Treatment options for RNV depend on the underlying cause of the condition and may include medications, laser therapy, or vitrectomy.
In summary, retinal neovascularization is a common complication of various retinal diseases that can lead to vision loss if left untreated. Early detection and prompt treatment are essential to prevent further damage and preserve visual function.
Symptoms of retinal perforations may include flashes of light, floaters, blurred vision, and loss of peripheral vision. These symptoms can be caused by a variety of factors, including age-related macular degeneration, diabetic retinopathy, and trauma to the eye.
Retinal perforations are typically diagnosed through a comprehensive eye exam, which may include imaging tests such as optical coherence tomography (OCT) and fluorescein angiography. Treatment for retinal perforations depends on the underlying cause of the condition, but may include laser surgery, cryotherapy, or vitrectomy.
In summary, retinal perforations are a serious condition that can cause significant vision loss if left untreated. Early detection and prompt treatment are essential to prevent long-term vision loss and improve outcomes for patients with retinal perforations.
There are two main types of DR:
1. Non-proliferative diabetic retinopathy (NPDR): This is the early stage of DR, where the blood vessels in the retina become damaged and start to leak fluid or bleed. The symptoms can be mild or severe and may include blurred vision, floaters, and flashes of light.
2. Proliferative diabetic retinopathy (PDR): This is the advanced stage of DR, where new blood vessels start to grow in the retina. These vessels are weak and can cause severe bleeding, leading to vision loss.
DR is a common complication of diabetes, and it is estimated that up to 80% of people with diabetes will develop some form of DR over their lifetime. The risk of developing DR increases with the duration of diabetes and the level of blood sugar control.
Early detection and treatment of DR can help to prevent vision loss, so it is important for people with diabetes to have regular eye exams to monitor their retinal health. Treatment options for DR include laser surgery, injections of anti-vascular endothelial growth factor (VEGF) medications, and vitrectomy, a surgical procedure to remove the vitreous gel and blood from the eye.
Preventing Diabetic Retinopathy
While there is no surefire way to prevent diabetic retinopathy (DR), there are several steps that people with diabetes can take to reduce their risk of developing this complication:
1. Control blood sugar levels: Keeping blood sugar levels within a healthy range can help to slow the progression of DR. This can be achieved through a combination of diet, exercise, and medication.
2. Monitor blood pressure: High blood pressure can damage the blood vessels in the retina, so it is important to monitor and control blood pressure to reduce the risk of DR.
3. Maintain healthy blood lipids: Elevated levels of low-density lipoprotein (LDL) cholesterol and lower levels of high-density lipoprotein (HDL) cholesterol can increase the risk of DR.
4. Quit smoking: Smoking can damage the blood vessels in the retina and increase the risk of DR.
5. Maintain a healthy weight: Obesity is a risk factor for DR, so maintaining a healthy weight can help to reduce the risk of this complication.
6. Get regular eye exams: Regular eye exams can help to detect DR in its early stages, when it is easier to treat and prevent vision loss.
Preventing Diabetic Retinopathy
While there is no cure for diabetic retinopathy (DR), there are several treatment options available to help manage the condition and prevent vision loss. These include:
1. Laser surgery: This is a common treatment for early-stage DR, where a laser is used to shrink abnormal blood vessels in the retina and reduce the risk of further damage.
2. Injection therapy: Medications such as anti-vascular endothelial growth factor (VEGF) injections can be used to shrink abnormal blood vessels and reduce swelling in the retina.
3. Vitrectomy: In severe cases of DR, a vitrectomy may be performed to remove scar tissue and blood from the center of the eye.
4. Blood pressure control: Maintaining healthy blood pressure can help to slow the progression of DR.
5. Blood glucose control: Keeping blood sugar levels under control can also slow the progression of DR.
6. Follow-up care: Regular follow-up appointments with an eye doctor are important to monitor the progress of DR and adjust treatment as needed.
Early detection and treatment of diabetic retinopathy can help to prevent vision loss and improve outcomes for individuals with this complication of diabetes. By managing blood sugar levels, blood pressure, and cholesterol, and by getting regular eye exams, individuals with diabetes can reduce their risk of developing DR and other diabetic complications.
Symptoms of macular edema may include blurred vision, distorted vision, blind spots, and sensitivity to light. Diagnosis is typically made through a comprehensive eye exam, including a visual acuity test and imaging tests such as optical coherence tomography (OCT).
Treatment for macular edema depends on the underlying cause of the condition. In some cases, medications such as anti-vascular endothelial growth factor (VEGF) injections or corticosteroids may be prescribed to reduce fluid buildup and swelling in the retina. In more severe cases, surgical intervention may be necessary, such as a vitrectomy to remove the vitreous gel and relieve pressure on the retina.
Prevention of macular edema includes managing underlying conditions such as diabetes and age-related macular degeneration, as well as maintaining regular eye exams to detect and treat any changes in the retina early on. Early detection and treatment can help prevent vision loss from macular edema.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
There are several types of ischemia, including:
1. Myocardial ischemia: Reduced blood flow to the heart muscle, which can lead to chest pain or a heart attack.
2. Cerebral ischemia: Reduced blood flow to the brain, which can lead to stroke or cognitive impairment.
3. Peripheral arterial ischemia: Reduced blood flow to the legs and arms.
4. Renal ischemia: Reduced blood flow to the kidneys.
5. Hepatic ischemia: Reduced blood flow to the liver.
Ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as CT or MRI scans. Treatment for ischemia depends on the underlying cause and may include medications, lifestyle changes, or surgical interventions.
Angiopoietin-related protein 2
Angiopoietin 1
Angiopoietin
Angiopoietin-related protein 1
Hes3 signaling axis
Nesvacumab
ANGPT4
Thomas N. Sato
TEK tyrosine kinase
Pericyte
Michele De Palma
Host response to cancer therapy
Endothelium
PTPRB
Hedgehog signaling pathway
ANGPT2
Angiopoietin-related protein 7
Vascular endothelial growth factor A
Tumor-associated macrophage
Methaneseleninic acid
Faricimab
Vascular endothelial growth factor
Ischemia-reperfusion injury of the appendicular musculoskeletal system
Schlemm's canal
Angiopoietin receptor
TNIP2
Weibel-Palade body
List of MeSH codes (D12.776)
MTOR inhibitors
Chromosome 9
ELF2
MECOM
GAB2
TIE1
TIMI
Milica Radisic
Proteases in angiogenesis
Laminin
ANGPTL4
ANGPTL8
GPIHBP1
FCN3
FCN1
GRLF1
Vanucizumab
N-Acetylmannosamine
Karen Lam (researcher)
Tumor Cell-Derived Angiopoietin-2 Promotes Metastasis in Melanoma - PubMed
Genetic variation implicates plasma angiopoietin-2 in the development of acute kidney injury sub-phenotypes - PubMed
Angiopoietin 2 displays a vascular endothelial growth factor dependent synergistic effect in hepatocellular carcinoma...
Angiopoietin-2 | Colorado PROFILES
Angiopoietin-2 mouse rat ELISA | Eagle Biosciences
Angiopoietin 2 stimulates TIE2-expressing monocytes to suppress T cell activation and to promote regulatory T cell expansion. ...
The Tie-2 ligand Angiopoietin-2 destabilizes quiescent endothelium through an internal autocrine loop mechanism | Journal of...
Associations of TP53 codon 72 polymorphism with complications and comorbidities in patients with type 1 diabetes | SpringerLink
Latest Articles : ASAIO Journal
Angiopoietins, Angiopoietin-like Proteins, and Receptors Research Areas: R&D Systems
Febrile Illness Evaluation in a Broad Range of Endemicities (FIEBRE) | LSHTM
A lymphatic defect causes ocular hypertension and glaucoma in mice - PubMed
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MeSH Browser
Papers in Vascular Biology Accordions - North American Vascular Biology Organization
Proteins4
- Two domains characterize the angiopoietin family of proteins: an N-terminal coiled-coil domain that mediates homo-oligomerization, and a C-terminal fibrinogen-like domain that binds Tie-2. (rndsystems.com)
- Leukocyte Immunoglogulin-like Receptors (LILRs), also called CD85 or Immunoglobulin-like Transcripts (ILTs), have recently been described as receptors for several Angiopoietin-like proteins. (rndsystems.com)
- Oligomerization of Angiopoietin-like proteins via the N-terminal coiled-coil domain is required to trigger LILR signaling. (rndsystems.com)
- Additional Angiopoietin-like proteins interact with various members of the LILR family to promote regulation of innate immunity. (rndsystems.com)
TIE28
- During angiogenesis, ANG2 exerts its effects via the angiopoietin-1/TIE2 receptor signaling system on endothelial cells. (eaglebio.com)
- Thus, in cancer, targeting the TIE2-Angiopoietin pathway has shown promising results in some preclinical and clinical trials, including studies on recurrent or metastatic breast and renal cell carcinomas. (eaglebio.com)
- Angiopoietin 2 stimulates TIE2-expressing monocytes to suppress T cell activation and to promote regulatory T cell expansion. (bvsalud.org)
- Here, we demonstrated that genetic disruption of the angiopoietin/TIE2 (ANGPT/TIE2) signaling pathway results in high IOP, buphthalmos, and classic features of glaucoma, including retinal ganglion degeneration and vision loss. (nih.gov)
- 21. Toll-like receptor 2 induced angiogenesis and invasion is mediated through the Tie2 signalling pathway in rheumatoid arthritis. (nih.gov)
- 24. A designed angiopoietin-2 variant, pentameric COMP-Ang2, strongly activates Tie2 receptor and stimulates angiogenesis. (nih.gov)
- 27. Tie1 regulates the Tie2 agonistic role of angiopoietin-2 in human lymphatic endothelial cells. (nih.gov)
- 32. Rat aorta-derived mural precursor cells express the Tie2 receptor and respond directly to stimulation by angiopoietins. (nih.gov)
Angiogenesis5
- Angiopoietin/Tie receptor signaling cascades are involved in fundamental angiogenesis events including vascular stabilization and remodeling, as well as recruitment of pericytes and smooth muscle cells. (rndsystems.com)
- 5. COMP-angiopoietin-1 promotes wound healing through enhanced angiogenesis, lymphangiogenesis, and blood flow in a diabetic mouse model. (nih.gov)
- 22. T11TS inhibits Angiopoietin-1/Tie-2 signaling, EGFR activation and Raf/MEK/ERK pathway in brain endothelial cells restraining angiogenesis in glioma model. (nih.gov)
- 35. Angiopoietin-2 TIEs up macrophages in tumor angiogenesis. (nih.gov)
- 39. Curcumin Suppresses Tumor Growth and Angiogenesis in Human Glioma Cells Through Modulation of Vascular Endothelial Growth Factor/ Angiopoietin-2/Thrombospondin-1 Signaling. (nih.gov)
Receptors2
- Some of the ligand/receptor signaling systems that we currently study include ephrins/Eph receptors, netrins/DCC/Unc5, NogoR/Nogo and angiopoietins/Ties. (sloankettering.edu)
- binds to the 3 major VEGF-A isoforms (eg, VEGF110, VEGF121, VEGF165), thereby preventing interaction with receptors VEGFR-1 and VEGFR-2. (medscape.com)
Pathway1
- 31. The Angiopoietin-2 and TIE Pathway as a Therapeutic Target for Enhancing Antiangiogenic Therapy and Immunotherapy in Patients with Advanced Cancer. (nih.gov)
Binds2
- It binds to the TIE-2 RECEPTOR without receptor stimulation and antagonizes the effect of ANGIOPOIETIN-1. (ucdenver.edu)
- Angiopoietin-2 present in the sample binds to the pre-coated antibody in the well. (eaglebio.com)
Ligand1
- These data reveal a pathogenetic and molecular basis for glaucoma and demonstrate the importance of angiopoietin ligand cooperation in the lymphatic endothelium. (nih.gov)
Endothelial-cell5
- Endothelial-cell monolayer integrity in this model is dependent on Tie-2 signaling, as evidenced by detaching endothelial cells following exposure to the small molecular weight Tie-2 inhibitor A-422885.66, which cannot be overcome by exogenous Ang-1. (biologists.com)
- Accordingly, exogenous Ang-2 rapidly destabilizes the endothelial layer, which can be observed within 30-60 minutes and leads to prominent endothelial-cell detachment within 4 hours. (biologists.com)
- Exogenous Ang-2-mediated endothelial-cell detachment can be rescued by Ang-1, soluble Tie-2 and vascular endothelial growth factor. (biologists.com)
- However, autocrine Ang-2-mediated endothelial-cell detachment cannot be blocked by soluble Tie-2. (biologists.com)
- Faricimab targets 2 distinct pathways - angiopoietin-2 (Ang-2) and vascular endothelial growth factor-A (VEGF-A). By inhibiting VEGF-A, faricimab suppresses endothelial cell proliferation, neovascularization and vascular permeability. (medscape.com)
Vascular5
- 2 Vascular Oncology and Metastasis, German Cancer Research Center, Heidelberg (DKFZ-ZMBH Alliance), Germany. (nih.gov)
- The angiopoietins Ang-1 and Ang-2 have been identified as ligands of the endothelial receptor tyrosine kinase Tie-2, which controls vascular assembly and endothelial quiescence. (biologists.com)
- Thus, stimulated release of endogenous Ang-2 or overexpression of Ang-2 in endothelial cells perturbs co-culture spheroid integrity, which can be rescued by exogenous Ang-1 and vascular endothelial growth factor. (biologists.com)
- The Role of Angiopoietin-2 in Vascular Calcification (Doctoral dissertation). (ucl.ac.uk)
- By inhibiting Ang-2, faricimab promotes vascular stability and desensitize blood vessels to the effects of VEGF-A. (medscape.com)
ELISA2
- The Angiopoietin-2 mouse rat ELISA is an enzyme immunoassay intended for the quantitative determination of mouse or rat angiopoietin-2 in serum or plasma. (eaglebio.com)
- The Eagle Biosciences Angiopoietin-2 mouse rat ELISA is for research use only and is not to be used in diagnostic procedures. (eaglebio.com)
Tumor growth1
- In addition, since an adequate blood supply is required for tumor growth, Angiopoietin/Tie receptor signaling is believed to play an important role in many cancer pathologies. (rndsystems.com)
ANGPT21
- Angiopoietin 2 (ANGPT2) is a proangiogenic cytokine whose expression is often upregulated by endothelial cells in tumors . (bvsalud.org)
Antibody2
- In a first step, STD/CTRL/Sample are pipetted into the wells of the microtiter strips, which are pre-coated with a recombinant monoclonal Angiopoietin-2 antibody. (eaglebio.com)
- Additionally, IL-2 producing T cells and plasma levels of IL-2 were positively correlated with antibody levels. (bvsalud.org)
Mutations1
- 2. Low frequency of PDCD10 mutations in a panel of CCM3 probands: potential for a fourth CCM locus. (nih.gov)
Antagonistic3
- The largely complementary phenotypes of Ang-1-deficient mice and Ang-2-overexpressing mice have led to an antagonistic model in which Ang-1 acts as Tie-2-activating agonist and Ang-2 acts as a Tie-2-inhibiting antagonist. (biologists.com)
- To date, no mechanistic equivalent of the antagonistic Ang-1/Ang-2 model has been established and the mechanisms of Ang-2 function in particular remain mysterious. (biologists.com)
- Taken together, the data demonstrate for the first time the antagonistic Ang-1/Ang-2 concept in a defined cellular model and identify Ang-2 as a rapidly acting autocrine regulator of the endothelium that acts through an internal autocrine loop mechanism. (biologists.com)
Receptor tyrosi1
- Angiopoietins, Ang-1, Ang-2, and Ang-3 (mouse)/Ang-4 (human), are natural ligands of the Tie-2 receptor tyrosine kinase, which is expressed primarily on endothelial cells and early hematopoietic cells. (rndsystems.com)
Deficiency2
- 18. Endothelial exocytosis of angiopoietin-2 resulting from CCM3 deficiency contributes to cerebral cavernous malformation. (nih.gov)
- It is indicated for seizures associated with cyclin-dependent kinase-like 5 (CDKL5) deficiency disorder (CDD) in patients aged 2 years and older. (medscape.com)
Descriptor1
- Angiopoietin-2" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (ucdenver.edu)
Protein5
- The potential role of angiopoietin-like protein-8 in type 2 diabetes mellitus: a possibility for predictive diagnosis and targeted preventive measures? (springer.com)
- The P53 protein is activated when DNA damage occurs by stress such as ultraviolet radiation, heat shock, growth factor withdrawal, hypoxia, and inflammation in various cells and tissues [ 2 ]. (springer.com)
- Iodine Status and Growth In 0-2-Year-Old Infants With Cow's Milk Protein Allergy. (uib.no)
- The first member of the Angiopoietin-like protein family to be discovered. (nih.gov)
- A circulating angiopoietin-like protein that is expressed in a variety of tissues in response to HYPOXIA . (nih.gov)
Mast1
- PTH-enhanced structural allograft healing is associated with decreased angiopoietin-2-mediated arteriogenesis, mast cell accumulation, and fibrosis. (ucdenver.edu)
VEGF2
- 29. Targeting the Angiopoietin-2/Tie-2 axis in conjunction with VEGF signal interference. (nih.gov)
- Indicated for treatment of neovascular (wet) AMD in patients who have previously responded to at least 2 intravitreal injections of a VEGF inhibitor. (medscape.com)
20173
Distinct1
- This heterogeneity has been explained in part by the identification of 2 distinct genes. (jci.org)
Human2
- 28. Angiopoietin-2 induces human glioma invasion through the activation of matrix metalloprotease-2. (nih.gov)
- The simian parasite Plasmodium knowlesi has recently been found to be a major cause of human malaria in Malaysian Borneo ( 1 , 2 ), with the disease also reported from southern and eastern Asia ( 3 ). (cdc.gov)
Closely1
- An angiopoietin that is closely related to ANGIOPOIETIN-1. (ucdenver.edu)
Patients3
- At most recent follow-up, patients needed mean of 5 treatments in first 2 y. (medscape.com)
- Subsequently, a prospective study from the Kapit District Hospital in Sarawak enrolled 107 persons with P. knowlesi monoinfection and demonstrated that 10 patients had severe disease as defined by World Health Organization (WHO) criteria, resulting in 2 deaths ( 2 ). (cdc.gov)
- Assessment of Angiopoietin-2 Single Nucleotide Polymorphism in Patients with Rheumatoid Arthritis. (cdc.gov)
Inflammation3
- 1. COMP-angiopoietin-1 ameliorates inflammation-induced lymphangiogenesis in dextran sulfate sodium (DSS)-induced colitis model. (nih.gov)
- 2. The Effect of Artemisinin on Inflammation-Associated Lymphangiogenesis in Experimental Acute Colitis. (nih.gov)
- 18. Carvacrol exhibits anti-oxidant and anti-inflammatory effects against 1, 2-dimethyl hydrazine plus dextran sodium sulfate induced inflammation associated carcinogenicity in the colon of Fischer 344 rats. (nih.gov)
Marker1
- Circulating angiopoietin-2 is a marker for early cardiovascular disease in children on chronic dialysis. (ucdenver.edu)
Role1
- Angiopoietin-2 may therefore play a role in down-regulation of BLOOD VESSEL branching and sprouting. (ucdenver.edu)
Results1
- Accelerated approval from the FDA was supported by interim results from the phase 2/3 STARBEAM study, which concluded that elivaldogene autotemcel may be an effective alternative to allogeneic stem-cell transplantation in boys with early stage CALD. (medscape.com)
Recombinant1
- The kit utilizes recombinant mouse Angiopoetin-2 as a calibrator. (eaglebio.com)
20191
- 2019-nCoV Vaccine mRNA-1273 mRNA vaccine against SARS-CoV-2 developed by Moderna. (nih.gov)
Expression1
- 34. Preliminary evidence of sustained expression of angiopoietin-2 during monocyte differentiation in chronic hepatitis C. (nih.gov)
10.11861
- doi: 10.1186/s13006-017-0112-2. (uib.no)
Molecular1
- Molecular Genetics and Metabolism, 105 (2), 255 - 262. (up.pt)
Mouse2
- This kit is a sandwich enzyme immunoassay for the quantitative determination of mouse/rat Angiopoietin-2 inserum and plasma samples. (eaglebio.com)
- The enzyme catalysed color change of the substrate is directly proportional to the amount of mouse/rat Angiopoietin-2 present in the sample. (eaglebio.com)
Vaccine1
- A viral vector vaccine designed against SARS-CoV-2 developed by Johnson & Johnson. (nih.gov)
Complex1
- Tie-1 may also act as an angiopoietin receptor, possibly in complex with Tie-2. (rndsystems.com)
Year1
- This graph shows the total number of publications written about "Angiopoietin-2" by people in this website by year, and whether "Angiopoietin-2" was a major or minor topic of these publications. (ucdenver.edu)
Directly1
- The concentration of Angiopoietin-2 in the sample is determined directly from the dose response curve. (eaglebio.com)