Heme oxygenase-1 is an inducible enzyme that catalyzes heme degradation and has been proposed to play a role in protecting cells against oxidative stress-related injury. We investigated the induction of heme oxygenase-1 by the tumor promoter arsenite in a chicken hepatoma cell line, LMH. We identified a heme oxygenase-1 promoter-driven luciferase reporter construct that was highly and reproducibly expressed in response to sodium arsenite treatment. This construct was used to investigate the role of mitogen-activated protein (MAP) kinases in arsenite-mediated heme oxygenase-1 gene expression. In LMH cells, sodium arsenite, cadmium, and heat shock, but not heme, induced activity of the MAP kinases extracellular-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38. To examine whether these MAP kinases were involved in mediating heme oxygenase-1 gene expression, we utilized constitutively activated and dominant negative components of the ERK, JNK, and p38 MAP kinase signaling pathways. Involvement

TY - JOUR. T1 - Heme oxygenase-1 is induced in glia throughout brain by subarachnoid hemoglobin. AU - Turner, Christopher P.. AU - Bergeron, Marcelle. AU - Matz, Paul. AU - Zegna, Angelo. AU - Noble, Linda J.. AU - Panter, S. Scott. AU - Sharp, Frank R. PY - 1998/3. Y1 - 1998/3. N2 - The heme oxygenase-1 gene, HO-1, induced by heme, ischemia, and heat shock, metabolizes heme to biliverdin, free iron, and carbon monoxide. Though the distribution of HO-1 has been described in normal rat brain, little is known about how extracellular heme proteins in the subarachnoid space distribute in brain. To address this issue, hemoglobin was injected into the cisterna magna of adult rats. Expression of HO-1 in these animals was compared with saline-injected, BSA-injected, and uninjected controls. Western blot analysis showed that 24 hours after injection oxyhemoglobin increased HO-1 levels approximately four- to fivefold in all brain regions studied compared with saline-injected and BSA-injected controls. In ...

HO-1 (haem oxygenase-1) catalyses the degradation of haem and possesses anti-inflammatory and cytoprotective properties. The role of inflammatory mediators in the pathogenesis of OA (osteoarthritis) is becoming increasingly appreciated. In the present study, we investigated the effects of HO-1 induction in OA and healthy HACs (human articular chondrocytes) in response to inflammatory cytokine IL-1 β (interleukin-1β) under hypoxic conditions. Hypoxia was investigated as it is a more physiological condition of the avascular cartilage. Hypoxic signalling is mediated by HIFs (hypoxia-inducible factors), of which there are two main isoforms, HIF-1α and HIF-2α. Normal and OA chondrocytes were stimulated with IL-1β. This cytokine suppresses HO-1 expression and exerts both catabolic and anti-anabolic effects, while increasing HIF-1α and suppressing HIF-2α protein levels in OA chondrocytes in hypoxia. Induction of HO-1 by CoPP (cobalt protoporphyrin IX) reversed these IL-1β actions. The ...

Heme oxygenase-1 (HO-1), an antioxidant defense enzyme, has been shown to protect against oxidant-induced liver injury. However, its role on liver fibrosis remains unclear. This study aims to elucidate the effect and the mechanism of HO-1 in nutritional fibrosing steatohepatitis in mice. Male C57BL/6J mice were fed with a methionine-choline deficient (MCD) diet for eight weeks to induce hepatic fibrosis. HO-1 chemical inducer (hemin), HO-1 chemical inhibitor zinc protoporphyrin IX (ZnPP-IX) and/or adenovirus carrying HO-1 gene (Ad-HO-1) were administered to mice, respectively. Liver injury was assessed by serum ALT, AST levels and histological examination; hepatic lipid peroxides levels were determined; the expression levels of several fibrogenic related genes were assayed by real-time quantitative PCR and Western blot. MCD feeding mice showed progressive hepatic injury including hepatic steatosis, inflammatory infiltration and fibrosis. Induction of HO-1 by hemin or Ad-HO-1 significantly attenuated the

TY - JOUR. T1 - Acetylation is essential for nuclear heme oxygenase-1-enhanced tumor growth and invasiveness. AU - Hsu, F. F.. AU - Chiang, M. T.. AU - Li, F. A.. AU - Yeh, C. T.. AU - Lee, W. H.. AU - Chau, L. Y.. N1 - Funding Information: This work was supported by the Ministry of Science and Technology Taiwan (MOST 103-2320-B-001-013-MY3). We thank IBMS proteomics core for the LC-MS analysis.. PY - 2017/8/28. Y1 - 2017/8/28. N2 - Overexpression of heme oxygenase-1 (HO-1), an endoplasmic reticulum-anchored enzyme, is observed in many cancers. HO-1 nuclear translocation has been shown to correlate with progression of several cancers. We recently reported that HO-1 is susceptible to intramembrane proteolysis and translocates to the nucleus to promote cancer growth and invasiveness without depending on its enzymatic activity. In the present study, we show that the HO-1 lacking C-terminal transmembrane segment (t-HO-1) was susceptible to acetylation by p300 and CREB-binding protein (CBP) histone ...

INTRODUCTION: Remifentanil preconditioning (RPC) can protect the heart from ischemia-reperfusion injury (IRI). Heme oxygenase-1 (HO-1) can also reduce the cardiac infarct size during ischemia reperfusion in vivo. Our aim was to investigate whether HO-1 expression participates in RPC cardio protection. METHODS: IRI was induced in male Sprague-Dawley rats (300g) by occluding the left coronary artery for 30 minutes followed by 2 hours of reperfusion. 6μg/kg/min remifentanil as administered in three infusion cycles of 5-min (RPC group). Hemin, an agonist of HO-1, 30mg/kg/d was given intraperitoneally for 2 days before RPC (RPC+hemin group). Tin Protoporphyrin IX (SnPP), which can inhibit HO-1 expression, was injected 0.7 mg/kg/day subcutaneously for 2 days before RPC (RPC+SnPP group). The non-operation group was marked as sham. In the control group, 0.9% saline replaced remifentanil. After the operation, the heart infarct size was determined by 2, 3, 5-triphenyltetrazolium staining. Expression of ...

Introduction: Heme oxygenase-1 (HO-1) is a cytoprotective enzyme induced by stress. Heart failure is a condition of chronic stress-induced remodeling and is often accompanied by comorbidities such as age and hypertension. HO-1 is known to be protective in the setting of acute myocardial infarction. The role of HO-1 in heart failure is not known, particularly in the setting of pressure overload.. Methods: Mice with alpha-myosin heavy chain restricted expression of HO-1 were aged for 1 year. In addition, mice underwent transverse aortic constriction (TAC) or were infused with isoproterenol (ISO) to induce heart failure.. Results: HO-1 transgenic mice developed spontaneous heart failure after 1 year compared to their wild-type littermates and showed accelerated cardiac dysfunction 2 weeks following TAC. Wild-type mice undergoing pressure overload demonstrated extensive interstitial fibrosis that was prevented by HO-1 overexpression, yet HO-1 transgenic mice had reduced capillary density, ...

We examined the effects of upregulation of heme oxygenase-1 (HO-1) in steatotic rat liver models of ex vivo cold ischemia/reperfusion (I/R) injury. In the model of ischemia/isolated perfusion, treatment of genetically obese Zucker rats with the HO-1 inducer cobalt protoporphyrin (CoPP) or with adeno …

Background & Aims Heme oxygenase-1 (HO-1) is an antioxidant defense and key cytoprotective enzyme, which is repressed by Bach1. MicroRNA-122 (miR-122) is specifically expressed and highly abundant in human liver and required for replication of hepatitis C virus (HCV) RNA. This study was to assess whether a specific miR-122 antagomir down-regulates HCV protein replication and up-regulates HO-1. Methods We transfected antagomir of miR-122, 2′-O-methyl-mimic miR-122, or non-specific-control antagomir (NSCA) into wild type Huh-7 cells or Huh-7 stably replicating HCV subgenomic core-NS3 (CNS3 replicon cells), or NS3-5B (9-13 replicon cells). Results Antagomir of miR-122 reduced the abundance of HCV-RNA by 64% in CNS3, and by 84% in 9-13 cells. In contrast, transfection with 2′-O-methlyl-mimic miR-122 increased HCV levels up to 2.5-fold; transfection with NSCA did not change the level of HCV. Antagomir of miR-122 also decreased Bach1 and increased HO-1 mRNA levels in CNS3, 9-13, and WT

Heme oxygenase-1 (HO-1) is a microsomal enzyme that degrades heme, a prosthetic group of the heme protein family (e.g., hemoglobin), into the bile pigment biliverdin. Biliverdin is subsequently converted to bilirubin, carbon monoxide, and reduced iron. Bilirubin has an anti-inflammatory effect and is part of the oxidative stress response due to its strong free radical scavenging activity, whereas carbon monoxide has a vasodilatory effect on organ blood flow ...

Heme oxygenase-1 (HO-1) is a microsomal enzyme that degrades heme, a prosthetic group of the heme protein family (e.g., hemoglobin), into the bile pigment biliverdin. Biliverdin is subsequently converted to bilirubin, carbon monoxide, and reduced iron. Bilirubin has an anti-inflammatory effect and is part of the oxidative stress response due to its strong free radical scavenging activity, whereas carbon monoxide has a vasodilatory effect on organ blood flow ...

Differences in microRNA (miRNA) expression after intracerebral hemorrhage (ICH) have been reported in human and animal models, and miRNAs are being investigated as a new treatment for inflammation and oxidative stress after ICH. In this study, we found that microRNA-183-5p expression was decreased in the mouse brain after ICH. To investigate the effect of miRNA-183-5p on injury and repair of brain tissue after ICH, saline, miRNA-183-5p agomir, or miRNA-183-5p antagomir were injected into the lateral ventricles of 8-week-old mice with collagenase-induced ICH. Three days after ICH, mice treated with exogenous miRNA-183-5p showed less brain edema, neurobehavioral defects, inflammation, oxidative stress, and ferrous deposition than control mice. In addition, by alternately treating mice with a heme oxygenase-1 (HO-1) inducer, a HO-1 inhibitor, a nuclear factor erythroid 2-related factor (Nrf2) activator, and Nrf2 knockout, we demonstrated an indirect, HO-1-dependent regulatory relationship between miRNA-183

Heme Oxygenase-1 Induction Improves Cardiac Function following Myocardial Ischemia by Reducing Oxidative Stress. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.

Conference Paper: Z-ligustilide protects neuronal PC12 cells from oxidative stress by inducing heme oxygenase-1 via the Nrf2 and PI3K/Akt mediated ...

Activation of heme oxygenase-1 (HO-1), a heme-degrading enzyme responsive to a wide range of cellular stress, is traditionally considered to convey adaptive responses to oxidative stress, inflammation and vasoconstriction. These diversified effects a

話としてすごすぎる Heme Oxygenase-1 Drives Metaflammation and Insulin Resistance in Mouse and Man: Cell http://t.co/vY5NIdx0Z1. ...

My laboratory investigates mechanisms of lung injury and cytoprotection during oxidant stress. Specifically, we have focused on the lung endothelium as a central mediator of lung injury and repair responses. We identified the importance of the stress-response protein heme oxygenase-1 (HO-1) and its gaseous reaction product, carbon monoxide (CO), in resisting oxidant-induced endothelial cell death via mitochondrial pathways. We found that a family of signaling molecules, mitogen-activated protein kinases (MAPKs), mediates HO-1s and COs protective effects as well as optimal IL-13-induced lung inflammation / remodeling and, more recently, critical innate immune responses. The innate immune system consists of pattern-recognition receptors called toll-like receptors (TLRs), of which TLR4 is the LPS-responsive receptor. We discovered that TLR4 is required for lung structural cell survival in aging and oxidant challenges. These studies represent important paradigm shifts in our understanding of TLRs ...

Background: PM2.5 (particles matter smaller aerodynamic diameter of 2.5 μm ) exposure, as one major environmental risk factor for the global burden of disease, is associated with high risks of respiratory diseases and lung cancer. Heme-oxygenase 1 (HMOX1) has been c...

Tumor-associated macrophages (TAMs) contribute to the maintenance of a strong immunosuppressive environment, supporting tumor progression and resistance to treatment. To date, the mechanisms that drive acquisition of these immunosuppressive features are still poorly defined. Heme oxygenase-1 (HO-1) is the rate-limiting enzyme that catabolizes free heme. It displays important cytoprotective, antiinflammatory, and antioxidant properties. A growing body of evidence suggests that HO-1 may also promote tumor development. Herein, we show that HO-1 is highly expressed in monocytic cells in the tumor microenvironment (TME) once they differentiate into TAMs. Deletion of HO-1 in the myeloid compartment enhances the beneficial effects of a therapeutic antitumor vaccine by restoring CD8+ T cell proliferation and cytotoxicity. We further show that induction of HO-1 plays a major role in monocyte education by tumor cells by modulating their transcriptional and epigenetic programs. These results identify HO-1 ...

Anti-inflammatory and immunomodulatory effects. The anti-inflammatory and immunomodulatory effect of MO is expressed through the activation or inhibition of different molecular pathways, involved in systemic inflammation. For instance, MO inhibits the nuclear factor-kappaB (NF-κB) pathway, whose activation promotes the transcription of proinflammatory cytokine genes such as tumor necrosis factor-α, IL-1β, IL-8.[23] The underlying reasons for the anti-inflammatory efficacy of MO therapy can therefore be found in a systemic reduction of inflammatory parameters such as IL-1.[24] On the other hand, MO stimulates the activation of the nuclear factor erythroid 2-related factor 2 pathway,[25] an intracellular transcription factor, binding to the anti-oxidant response elements nuclear regions encoding for antioxidants enzymes such as superoxide dismutase, catalase and heme oxygenase-1. Heme oxygenase-1 is a microsomal enzyme that catalyzes the degradation of haeme and produces carbon monoxide, which ...

A direct change at the Michael system can also alter the reactivity and thus the biological activity of enones. The approach of modifying the α-position of the α,β-unsaturated carbonyl system is a promising concept, because it should lead to a direct and straightforward influence on its reactivity. The chemical reactivity of α-X-enones depends on the nature of the α-substituent, thus activating or deactivating the Michael acceptor reactivity toward thiols responsible for a biological response. The influence of different α-X-substituted 2,3,4,4-tetramethoxychalcones (α-X-TMCHs) on the induction of HO-1 protein expression and HO-1 enzymatic activity and on the other hand the inhibition of NO production, regulated by iNOS was determined in RAW264.7 murine macrophages. A clear correlation could be established between the reactivity of α-X-TMCHs, demonstrated by their thia-Michael addition reaction with cysteamine (k2 values) and their biological activity. The results demonstrate that a ...

Projekt „Repozytorium otwartego dostępu do dorobku naukowego i dydaktycznego UJ współfinansowany w ramach poddziałania 2.3.1 „Cyfrowe udostępnianie zasobów nauki Programu Operacyjnego Polska Cyfrowa z Europejskiego Funduszu Rozwoju Regionalnego i budżetu państwa na podstawie umowy o dofinansowanie nr POPC.02.03.01-00-0030/17-00 ...

Taylor, N, Kremser, I, Auer, S, Hoermann, G, Greil, R, Haschke-Becher, E, Esterbauer, H, Kenner, L, Oberkofler, H.. http://www.ncbi.nlm.nih.gov/pubmed/27798431. ...

The biological function of carbon monoxide (CO) and its versatile role as a cellular messenger in mammals is presently attracting the interest of several investigators. CO regulates vessel tone and blood pressure (Motterlini et al., 1998; Wang, 1998), exerts anti-inflammatory actions (Otterbein et al., 2000), inhibits platelet aggregation (Brune and Ullrich, 1988), and acts as a signaling mediator in both apoptotic and antiapoptotic processes (Song et al., 2004; Zhang et al., 2004). The importance of CO in biology and medicine can be better appreciated by considering the multifunctional activities of heme oxygenase-1 (HO-1), a redox-sensitive-inducible enzyme that generates CO upon degradation of heme during conditions of intense oxidative or nitrosative stress (Motterlini et al., 2002c). Indeed, the induction of HO-1 seems to be central in the adaptation of tissues to a multitude of threatening conditions (Otterbein et al., 2003b). The signaling effects elicited by increased CO production in ...

This research analyzed the effect of β-glucan that is expected to alleviate the production of the inflammatory mediator in a macrophagocyte, which was processed by the lipopolysaccharide (LPS) of Escherichia, a pathogen related to allergy. The incubated layer was used for a nitric oxide (NO) analysis. The DNA-binding activation of the small unit of NF-κB was measured using the ELISA-based kit. In the RAW264.7 cells that were vitalized by E.coli LPS, the β-glucan inhibited both the combatant and rendering phases of the inducible NO synthase (iNOS)-derived NO. β-glucan increased the expression of the heme oxygenase-1 (HO-1) in the cell that was stimulated by E.coli LPS, and the HO-1 activation was inhibited by the SnPP. This shows that the NO production induced by LPS is related to the inhibition effect of β-glucan. The phosphorylation of JNK and the p38 induced by the LPS were not influenced by the β-glucan, and the IκB-α decomposition was not influenced either. Instead, β-glucan ...

A)Survival of Plasmodium infected Hbwt (n = 91) and HbS (n = 76) mice (10 independent experiments with survival advantage p , 0.05). Grey shading: expected time of ECM. HbS mice have a clear survival advantage. (B) Brain malaria-specific (H-2Kb/SSIEFARL Pentamer+ ) CD8+ T cell numbers infected Hbwt and HbS mice, 5 days after Plasmodium infection. Dots represent single mice (n = 4 -14/group). Red lines represent mean values. There are lower numbers of brain-infiltrating malaria-specific T cells in the HbS mice. (C) Mean brain edema in naive versus infected Hbwt and HbS mice ± standard deviation (n=4/group), 5 days after Plasmodium infection. Hbwt mice have significantly more edema than HbS mice. ns: not significant.. ECM pathology has previously been attributed to cytotoxic accumulation of free heme. Via a series of mouse crosses, Ferriera et al were able to establish how HbS counteracts heme accumulation. HbS induces expression of heme-oxygenase-1 (HO-1) in hematopietic cells. HO-1 -deficient ...

The aim of this thesis was to investigate both the early and late effects of cigarette smoke and nitrogen dioxide (NO2) exposure and the potential dampening effects of heme oxygenase-1 (HO-1) in animal models for COPD. Additionally, we investigated the role of the specific immune response in the inflammatory response in COPD, i.e. the involvement of B cells and regulatory T cells ...

抗氧化力的提升在癌症的預防上扮演著重要的角色。藉由提升phase II 解毒及抗氧化酵素之表現，例如 glutathione S-transferase、quinone reductase 及 heme oxygenase-1 (HO-1) 等等，可以促進環境中致癌物質的排除。Antioxidant responsive element (ARE) 座落在這些重要酵素基因之上游，並且會受到許多外來毒物及食品中具有功能性之化合物所活化。目前已有許多研究指出這些物質乃經由 MAPK、PI3K 及 PKC 等路徑來活化轉錄因子 Nrf2 的活化進而啟動下游基因之表現。花青素是屬於類黃酮化合物群，具有其多功能特性，包含抗發炎、預防心血管疾病、抗癌以及抗氧化等功效，然而目前尚缺乏對於花青素提升解毒及抗氧化酵素表現之直接證據。本研究計畫擬分三年進行，第一年選取數種天然存在之花青素，探討其對於提升肝細胞 ARE ...

This review is intended to stimulate interest in the effect of increased expression of heme oxygenase-1 (HO-1) protein and increased levels of HO activity on ...

Hamdulay, S S and Wang, B F and Birdsey, G M and Ali, F and Dumont, O and Evans, P C and Haskard, D O and Wheeler-Jones, C P D and Mason, J C (2010) Celecoxib activates PI-3K/Akt and mitochondrial redox signaling to enhance heme oxygenase-1-mediated anti-inflammatory activity in vascular endothelium. FREE RADICAL BIOLOGY AND MEDICINE, 48 (8). pp. 1013-1023. ...

No satisfactory technique yet exists in combat models for treating one major area of command decision making: the formulation and modification of concepts

HMOX1 (heme oxygenase (decycling) 1) is a human gene that encodes for the enzyme heme oxygenase 1 (EC 1.14.99.3). Heme oxygenase mediates the first step of heme catabolism, it cleaves heme to form biliverdin. Heme oxygenase, an essential enzyme in heme catabolism, cleaves heme to form biliverdin, carbon monoxide, and ferrous iron. The biliverdin is subsequently converted to bilirubin by biliverdin reductase. Heme oxygenase activity is induced by its substrate heme and by various nonheme substances. Heme oxygenase occurs as 2 isozymes, an inducible heme oxygenase-1 and a constitutive heme oxygenase-2. HMOX1 and HMOX2 belong to the heme oxygenase family. The HMOX gene is located on the long (q) arm of chromosome 22 at position 12.3, from base pair 34,101,636 to base pair 34,114,748. Heme oxygenase-1 deficiency The ability of oxygenase 1 to catabolize free heme and produce carbon monoxide (CO) gives its anti-inflammatory properties by up-regulation of interleukin 10 (IL-10) and interleukin 1 ...

Resveratrol (3,4,5-trihydroxy-trans-stilbene) is a secondary plant metabolite which is highly abundant in red grape skin and red wine [1]. Other dietary sources of resveratrol comprise berries, and peanuts [2, 3]. Although controversially discussed it has been recently shown that resveratrol may increase life span in model organisms such as Caenorhabditis elegans and Drosophila melanogaster [4-6]. The underlying mechanisms by which resveratrol may mediate beneficial effects have yet not been fully understood and may be partly related to its ability to induce phase II and antioxidant enzymes including heme oxygenase-1 and paraoxonase-1.. Heme oxygenase-1 (HO-1), is an inducible enzyme that catalyzes the rate-limiting step in the oxidative degradation of cellular heme that liberates iron, carbon monoxide (CO), and biliverdin. HO-1 exhibits antioxidant, anti-inflammatory and other cytoprotective functions [7].. Paraoxonase-1 (PON1) is a HDL associated serum enzyme which is mainly synthesized in ...

The IUPHAR/BPS Guide to Pharmacology. cobalt protoporphyrin IX ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs.

Activation of heme oxygenase-1 (HO-1) has been proved to reduce damages to the liver in ischemia reperfusion injury. The objective of present study was to determine whether clinic relevant doses of isoflurane treatment could be sufficient to activate HO-1 inducing, which confers protective effect against hepatic ischemia-reperfusion injury. The hepatic artery and portal vein to the left and the median liver lobes of forty male Sprague-Dawley rats were occluded for 60 minutes. Reperfusion was allowed for 4 hours before the animal subjects were sacrificed. Six groups (n = 12) were included in the study. A negative control group received sham operation and positive control group a standard ischemia-reperfusion regimen. The third group was pretreated with isoflurane prior to the ischemia-reperfusion. The fourth group received an HO-1 inhibitor zinc protoporphyrin (Znpp) prior to the isoflurane pretreatment and the ischemia-reperfusion. The fifth group received Znpp alone before ischemia-reperfusion

Activation of the proto-oncogene ras may play a critical role in the development and rapid progression of different types of human cancers, including renal cancer. It has been shown that the Ras pathway can mediate pro-survival signals in cancer cells by inhibiting cellular apoptosis. It is established that the cytoprotective enzyme heme oxygenase-1 (HO-1) is over-expressed in several cancers, and may play a significant role in the growth and metastasis of tumors by inducing cell survival pathways. However, it is not known if there is an association between Ras activation and HO-1 over-expression in cancer. We have recently demonstrated that the treatment of human renal cancer cells with the immunosuppressive agent cyclosporine may activate the H-Ras pathway, and promote a rapid progression of the disease. We have also shown that HO-1 is over-expressed in human renal cancer, and plays a key role in the survival of renal cancer cells by inhibiting cellular apoptosis. Here, we wished to analyze if ...

misc{7862195, abstract = {Acute or chronic inflammation in the prostate is implicated in pathogenesis of benign prostate hyperplasia (BPH) as well as development of prostatic intraepithelial neoplasia (PIN) and prostate cancer (PCa). Chronic prostatitis (inflammation in the prostate) is associated with high morbidity and negatively impacts life quality. Macrophages are critical regulators of inflammatory processes and are early immune cells responders. Among macrophage-associated genes, the stress-induced enzyme heme oxygenase-1 (HO-1), which degrades heme to carbon monoxide (CO), biliverdin and iron, has strong immunomodulatory effects in in vitro and in vivo disease models. In this study, we investigated the specific role of HO-1 in macrophages on modulation of prostate inflammation. We established a mouse model of bacterial prostatitis in wild type mice, and evaluated the role of HO-1 in pathogen-induced prostate inflammation by using mice with conditional deletion of HO-1 in myeloid cells ...

Purpose: Diabetic retinopathy (DR) is a progressive neurodegenerative disease and a leading cause of blindness. Overexpression of Heme Oxygenase-1(HO-1) by hemin induction protected retinal ganglion cells in diabetic retinopathy through anti-inflammatory, anti-apoptotic, and anti-proliferative effects. We investigated microRNA (miRNA) alterations in DR after hemin treatment with specific focus on miR-126, and its downstream target, HO-1.. Methods: miRNA expression profiling microarray (Affymetrix MicroRNA 2.0 Array) was used to examine the retinas of treated and non-treated streptozotocin- induced diabetic rats. Expressions of specific miRNAs were verified with PCR in the rat retina and in glucose-exposed endothelial cells. A target search, based on sequence complementarities, identified specific targets. We analyzed mRNA levels and protein expression in endothelial cells from large vessels and retinal capillaries and in the rat retina, with or without injection of miR-126 mimic or antagomir. ...

TY - JOUR. T1 - Down-regulation of heme oxygenase-1 by hepatitis C virus infection in vivo and by the in vitro expression of hepatitis C core protein. AU - Abdalla, Maher Y.. AU - Britigan, Bradley E.. AU - Wen, Feng. AU - Icardi, Michael. AU - McCormick, Michael L.. AU - LaBrecque, Douglas R.. AU - Voigt, Michael. AU - Brown, Kyle E.. AU - Schmidt, Warren N.. N1 - Funding Information: Financial support: Veterans Administration (Merit Review grants to B.E.B., M.L.M., and K.E.B.); National Institutes of Health (grants RO1 AA13215-01 and RO3 DK54842-03 to W.N.S. and RO1 AI34954 to B.E.B.); University of Iowa Carver Trust Foundation (to W.N.S. and B.E.B.).. PY - 2004/9/15. Y1 - 2004/9/15. N2 - Antioxidant enzymes, including heme oxygenase (HO)-1, are an important line of defense against oxidant-mediated liver injury. Because hepatitis C virus (HCV) infection appears to increase the production of oxidants, we evaluated levels of antioxidant enzymes and HO-1 in liver-biopsy samples from HCV-infected ...

Abstract: : Purpose: To evaluate the expression of heme oxygenase-1 (HO-1), which is a heme-catabolizing enzyme induced by oxidative stress and acts against oxidant-induced tissue injury, on ischemia-reperfusion injury in the rat retina. Methods: Retinal ischemia was induced in male 8weeks SD rats by increasing the intraocular pressure to 110 mmHg for 45 minutes. At 6, 12, 24, and 48 hours after reperfusion, rat eyes were enucleated. Expression of HO-1 and HO-2, a constitutive isoform, in mRNA level in the retina was determined by using RT-PCR and that of protein levels were also studied by using Western blotting analysis. For immunohistochemical double-labeling, sections were incubated with antibodies against HO-1 and S-100. To evaluate possible neuroprotective effects of hemin, an inducer of HO-1, we injected 150 mg/kg of hemin intraperitoneally before the ischemia. The degree of retinal damage was assessed by electroretinogram (ERG) recording on 1, 2 and 4 weeks thereafter, by measuring the ...

In the study, researchers gave ginkgo biloba EGb 761 - a lab-quality form of the extract - to normal mice and HO-1 knockout mice, mice lacking the gene that produces the enzyme heme oxygenase-1(HO-1). HO-1 breaks down heme, a common iron molecule found in blood, into carbon monoxide, iron and biliverdin. HO-1 has been shown to act as an antioxidant and have a protective effect against inflammation in animal models. Doré and his team gave 100 milligrams per kilogram of EGb 761 extract orally once daily for seven days before inducing stroke in the mice by briefly blocking an artery to one side of the brain. After stroke induction, the mice were tested for brain function and brain damage. One such test, for example, involves running patterns, another tests reaction to an external stimulus. Similar tests were conducted on mice that did not receive the ginkgo extract. Neurobehavioral function was evaluated before the study and at 1, 2 and 22 hours after stroke using a four-point scale: (1) no ...

Abstract: Many End staged Renal Diseased and hemodialysis patients are in a state of chronic inflammation induced by the dialysis process which further enhances oxidative stress. The study aim was to explore the critical role of Heme oxygenase-1, a potent antioxidant, in patients subjected to various dialysis conditions. The study population contained randomly selected end-staged renal failure patients (n = 64) who have been treated by hemodialysis for at least 6 months, between the age group of 20-50 with creatinine levels greater than 5 mg dL-1. About 20 samples were collected from predialysis patients, 22 samples were collected from patients undergoing dialysis and 22 samples were collected from post dialysis patients. The samples were subjected to antioxidant enzyme analysis followed by flow cytometric and immunoflouroscence studies HO-1 expression was found to be elevated in all the dialysis conditions but higher elevation was observed in post dialysis patients. The results suggest that ...

TY - JOUR. T1 - Deletion of caveolin-1 protects against oxidative lung injury via up-regulation of heme oxygenase-1. AU - Jin, Yang. AU - Hong, Pyo Kim. AU - Chi, Minli. AU - Ifedigbo, Emeka. AU - Ryter, Stefan W.. AU - Choi, Augustine M.K.. PY - 2008/8/1. Y1 - 2008/8/1. N2 - Acute lung injury (ALI) is a major cause of morbidity and mortality in critically ill patients. Hyperoxia causes lung injury in animals and humans, and is an established model of ALI. Caveolin-1, a major constituent of caveolae, regulates numerous biological processes, including cell death and proliferation. Here we demonstrate that caveolin-1-null mice (cav-1-/-) were resistant to hyperoxia-induced death and lung injury. Cav-1-/- mice sustained reduced lung injury after hyperoxia as determined by protein levels in bronchoalveolar lavage fluid and histologic analysis. Furthermore, cav-1 -/- fibroblasts and endothelial cells and cav-1 knockdown epithelial cells resisted hyperoxia-induced cell death in vitro. Basal and ...

Markovitch, D., Tyrrell, R. M. and Thompson, D., 2005. Heme oxygenase-1 expression in human lymphocytes and resistance to oxidative stress following exercise. FASEB Journal, 19 (4), A131-A131.. ...

Iron is indispensable to living organisms. Iron homeostasis is orchestrated both at the cellular and the systemic level, and liver plays a central role in the regulation of iron metabolism. An increasing number of genes associated with hepatic iron transport or regulation have been identified. Heme oxygenase-1(HO-1) and lactoferrin (Ltf) are among these genes known to regulate iron metabolism at cellular and systemic levels, respectively. Heme-oxygenase-1 is an intracellular positive acute phase protein and regulates one of the pathways that hepatic cells utilize to acquire free iron. The cytokines regulating HO-1 gene expression in liver and in other organs like muscle are only partially known. Moreover, lactoferrin serum concentration is known to increase under acute phase conditions, but the site of synthesis in not known.In the current work we investigated the changes in HO-1 and Ltf gene expression during turpentine oil- and LPS-induced acute phase reaction (APR). Cytokines are the core ...

1J02: Crystal Structures of Ferrous and CO-, CN(-)-, and NO-Bound Forms of Rat Heme Oxygenase-1 (HO-1) in Complex with Heme: Structural Implications for Discrimination between CO and O(2) in HO-1.

Post-liver transplantation acute lung injury (ALI) severely affects patients survival, whereas the mechanism is unclear and effective therapy is lacking. The authors postulated that reperfusion-induced increased oxidative stress plays a critical role in mediating post-liver transplantation ALI and that induction of heme oxgenase-1 (HO-1), an enzyme with anti-oxidative stress properties, can confer effective protection of lung against ALI. Male Sprague-Dawley rats underwent autologous orthotopic liver transplantation (OALT) in the absence or presence of treatments with the selective HO-1 inducer (Hemin) or HO-1 inhibitor (ZnPP). Lung tissues were collected at 8 h after OALT, pathological scores and lung water content were evaluated; survival rate of rats was analyzed; protein expression of HO-1 was determined by western blotting, and nuclear translocation of Nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor(NF)-κB p65 were detected by Immunofluorescence staining. The inflammatory

Redox homeostasis and the expression of antioxidant genes in visceral fat influence adiponectin release and inflammatory cytokines, TNFα and IL-6 levels. The redox state of visceral fat may also be a determining factor in insulin resistance, glucose intolerance and vascular dysfunction.. Aim: To examine the expression of stress response genes in visceral fat including glutathione s. transferase 1, (GST1), NAD (P) H-1 dehydroxygenase quinine 1 (Nq1), thioredoxin reductase 1 (TxR1) and heme oxygenase-1 (HO-1) in fat tissues of obese mice to assess upregulation of these genes affected insulin sensitivity and inflammatory cytokine levels.. Methods: Male lean and obese (ob/ob) mice (11 weeks old) were treated with either cobalt protoporphyrin (CoPP), i.p., 3 mg/kg or vehicle solution for 6 weeks. Serum levels of adiponectin, IL-1β, IL-6 were determined. Visceral fat GST1, Nq1, TxR1 and HO-1 levels were measured. Insulin resistance and glucose tolerance, adipocyte cell size and visceral and ...

The present study demonstrates a function of HO-1 activity as a potent host defense factor for HIV-1 infection. Our results clearly show that activation of HO-1 by its substrate hemin protected them against HIV infection with various clinical HIV isolates, including some of those that developed resistance to conventional antiretroviral drugs. In vivo, hemin administration in humanized NOD-SCID mice substantially suppressed HIV replication. These findings suggest that the HO-1 inducer, hemin, is a potentially effective endogenous biologic in inducing a host defense response against HIV infection. A critical component of a variety of proteins, including hemoglobin, hemin has been shown to exert numerous beneficial physiological functions (25). After being approved by the Food and Drug Administration, several formulations of hemin have been used since the 1970s to successfully treat acute porphyries, to control liver allograft failure due to recurrence of erythopoietic protophoria, and in patients ...

We have demonstrated that hypoxia-inducible HO-1 plasmid modification of MSCs enhances their survival in ischemic myocardium by real-time PCR assay. Moreover, we showed that the mechanism for enhancing grafted MSC survival is related to role of HO-1 in antiapoptosis and anti-inflammatory in ischemia myocardium. Mesenchymal stem cells treated with hypoxia-regulated HO-1 plasmid also attenuate LV remodeling and improve LV function, which is probably due to reduced apoptosis of grafted MSCs and reduced apoptosis in the host heart. These data suggest that hypoxia-regulated HO-1 plasmid gene modification of graft stem cells could be of significant value in improving the effectiveness of cell therapy in ischemic hearts.. The acute donor stem cell death that occurs immediately after engraftment is thought to have a major negative impact on the ensuing graft size and high level of cell death within four days after grafting into injured hearts (5). To reduce this attrition, the molecular mechanisms for ...

The IL-10 promoter is regulated through the p38 MAPK pathway in human macrophages (40). Our results demonstrated that acute ethanol treatment increased the levels of phosphorylated p38 in the same LPS-stimulated human monocytes that showed increased IL-10 and reduced TNF-α production. These effects of acute ethanol in our experiments were similar to the effects of CO, a product of HO-1 activation on monocytes (13). Consistent with the previously described role of p38 MAPK activation in IL-10 induction, inhibition of p38 activity with SB203580 prevented ethanol-induced augmentation of monocyte IL-10 production (28, 40). Activation of p38 MAPK has been shown to induce HO-1 expression in various cell types including macrophages (13), hepatocytes (24), pulmonary epithelial cells (41), and vascular cells (42). Our studies revealed that augmentation of p38 MAPK phosphorylation contributed to alcohol-induced HO-1 activation in LPS-stimulated monocytes. Recent studies demonstrated that transcriptional ...

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Parkinsons Disease is a peer-reviewed, Open Access journal that publishes original research articles, review articles, and clinical studies related to the epidemiology, etiology, pathogenesis, genetics, cellular, molecular and neurophysiology, as well as the diagnosis and treatment of Parkinsons disease.

Heme oxygenase-1 (HO-1, EC 1.14.99.3) is a key enzyme in the cellular response to tissue injury and oxidative stress. It oxidizes heme, a pro-oxidant and toxic species, to biliverdin, CO, and free iron. Cytoprotection during the heat shock response is a complex phenomenon involving multiple inducible mechanisms. Several important pathways involving serine/threonine kinases mediate the induction of HO-1 in response to external stimuli. The objective of the present study was to investigate the mechanism of HO-1 induction during cadmium (Cd)-induced oxidative stress and apoptosis in the lymphocyte B cell line BJAB. To examine the signal pathways involved in HO-1 expression, cells were pre-treated with various inhibitors of key signaling molecules. Increased DNA fragmentation and caspase-3 activity were observed in BJAB cells exposed to 5-40 μM CdCl2 revealing that Cd induced apoptosis in these cells. Our results indicate that Cd also induces HO-1 expression which is modulated by the thiol redox status,

Heme oxygenase-1 (HO-1) is an inducible, detoxifying enzyme that is critical for limiting oxidative stress, inflammation, and cellular injury within the CNS and other tissues. Here, we demonstrate a deficiency of HO-1 expression in the brains of HIV-infected individuals. This HO-1 .... ...

Heme oxygenase-1 (HO-1) is a tension response antioxidant enzyme which catalyzes the degradation of heme released during irritation. activity or considerably restrict bacterial development in liquid lifestyle. Together, the above mentioned results reveal mammalian HO-1 being a potential focus on for host-directed monotherapy and adjunctive therapy of tuberculosis and recognize the immune system 911417-87-3 response as a crucial regulator of the function. IMPORTANCE There is absolutely no dependable vaccine against tuberculosis (TB), and regular antibiotic therapy can be implemented at least 6?a few months. This extended treatment period can result in noncompliance leading to relapsed disease aswell as the introduction of multidrug level of resistance. Thus, there can be an urgent dependence on improved healing regimens that may quicker and effectively control in contaminated patients. Right here, we explain a potential technique for dealing with TB predicated on pharmacological inhibition from ...

CD36 is a membrane glycoprotein expressed on platelets, monocytes, macrophages, and several other cell types that was recently demonstrated to be involved in platelet activation in response to oxidized phospholipids, including oxidized LDL. Although the role of CD36 in other vascular cells has not been well defined, previous studies have demonstrated that cd36-knockout (cd36-/-) mice have prolonged thrombosis times after vascular injury, which can be protective in the state of hyperlipidemia. Here, we found significantly less ROS in the vessel walls of cd36-/- mice compared with WT after chemically induced arterial injury, suggesting that CD36 may contribute to ROS generation in the VSMCs themselves. Gene expression analysis revealed that the antioxidant enzymes peroxiredoxin-2 (Prdx2) and heme oxygenase-1 were upregulated in cd36-/- VSMCs. Molecular dissection of the pathway in isolated mouse VSMCs revealed CD36 ligand-dependent induction of Fyn phosphorylation, with subsequent phosphorylation ...

Long wave UVA radiation (340-400 nm) causes detrimental as well as beneficial effects on human skin. Studies of human skin fibroblasts irradiated with UVA demonstrate increased expression of both anti-fibrotic heme oxygenase-1 (HO-1) and matrix metalloproteinase 1 (MMP-1). The use of UVA -induced MMP-1 is well studied in treating skin ...

Wenzel P, Rossmann H, Müller C, Kossmann S, Oelze M, Schulz A, Arnold N, Simsek C, Lagrange J, Klemz R, Schönfelder T, Brandt M, Karbach SH, Knorr M, Finger S, Neukirch C, Häuser F, Beutel ME, Kröller-Schön S, Schulz E, Schnabel RB, Lackner K, Wild PS, Zeller T, Daiber A, Blankenberg S, Münzel T. 2015. Heme oxygenase-1 suppresses a pro-inflammatory phenotype in monocytes and determines endothelial function and arterial hypertension in mice and humans. European heart journal 36:3437-3446. 2015 ...

Synthesis of some sulfonamide incorporating enaminone, quinolone moieties and thiazoloquinazoline derivative induce the cytoprotective enzyme NAD(P) H: Quinone Oxidoreductase 1., M

Purified Recombinant Human HMOX2 Protein, Myc/DDK-tagged, C13 and N15-labeled from Creative Biomart. Recombinant Human HMOX2 Protein, Myc/DDK-tagged, C13 and N15-labeled can be used for research.