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Validated All-in-One™ qPCR Primer for HMOX1(NM_002133.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
Heme oxygenase, an essential enzyme in heme catabolism, cleaves heme to form biliverdin, which is subsequently converted to bilirubin by biliverdin reductase, and carbon monoxide, a putative neurotransmitter. 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. [provided by RefSeq].
Gene References into function
- Expression and regulation in healthy lung and interstitial lung disorders
- Gene transfection of H25A mutant heme oxygenase-1 protects cells against hydroperoxide-induced cytotoxicity
- Induction of HO-1 mRNA and protein expression in cultured endothelial cells by the active pentaerythrityl tetranitrate metabolite pentaerythrityl trinitrate is followed by increased cellular resistance to oxidant injury.
- Has a significant role in endothelial cell cycle progression
- Heme oxygenase-1, a protective gene that prevents the rejection of transplanted organs.
- This enzyme performs the seemingly lackluster function of catabolizing heme to generate bilirubin, carbon monoxide, and free iron.
- protection of grafts by this enzyme and its toxic product carbon monoxide
- Rickettsia rickettsii infection of culture human endothelial cells induces heme oxygenase 1 expression
- hHO-1 is potentially able to reduce the risk factors of atherosclerosis, partially due to its cellular protection against oxidative injury and to its inhibitory effect on cellular proliferation
- Exposure of endothelium to sublethal concentrations of heme-oxidized LDL leads to induction of both HO-1 and ferritin, leading to cytotoxicity.
- transcriptional activation of the human haem oxygenase-1 gene promoter in a hepatoma cell line
- microsatellite polymorphism in promoter of heme oxygenase-1 gene is associated with susceptibility to coronary artery disease in type 2 diabetic patients
- expression in colon carcinoma cells exposed to pyrrolidine dithiocarbamate
- Patients with AAA were less frequently carriers of short repeats in the HO-1 gene promoter than patients with atherosclerosis or healthy subjects. Short alleles facilitating upregulation of HO-1 may be a protective anti-inflammatory factor against AAA.
- HO-1 regulates the cell cycle in vascular endothelial and smooth muscle cells
- Abnormal reduction in endogenous heme oxygenase on the surface of placental trophoblasts may be one of the important mechanisms for the onset of intrauterine growth retardation.
- TGF-beta1 is a potent inducer of HO-1; the signaling pathway by which TGF-beta1 regulates HO-1 expression in human lung epithelial cells
- results indicate that prolonged overexpression of HO-1 ultimately decreases soluble guanylate cyclase activity by limiting the availability of cellular heme
- Length polymorphism in the HO-1 gene promoter is related to coronary artery disease susceptibility in Japanese people who also have coronary risk factors such as hypercholesterolemia, diabetes, and smoking.
- induction of HO-1 gene mediates protection against oxidants and increases cell survival by a mechanism independent of telomerase enzyme activity
- Heme oxygenase 1 mediates the immunomodulatory and antiapoptotic effects of interleukin 13 gene therapy in vivo in rats and in vitro in human cells.
- HO-1 mitigates the TNF-alpha-mediated changes in cell cycle progression and apoptosis, perhaps by a decrease in the levels of COX activity
- This enzyme is expressed in heart transplant recipients during acute rejection episodes, along with apoptosis.
- HO-1 has a specific conformation that allows tight binding to nitric oxide, which may contribute to the pleiotropic responses to NO and CO
- CYP2E1 overexpression up-regulates both non-specific delta-aminolevulinate synthase and this enzyme in a human hepatoma cell line.
- gene expression regulation used as a possible assessment for antioxidant capacity in Alzheimer's disease
- This enzyme is expressed in heart transplant recipients during acute rejection episodes.
- comparison of heme-gree and -bound crystal structures
- Polymorphism in HMOX1 might be associated with development of emphysematous changes in the lung.
- gene induction by glucose deprivation is mediated by reactive oxygen species via the mitochondrial electron-transport chain
- determination of binding sites on cytochrome P450 reductase and biliverdin reductase
- HO-1 expression occurs in human epidermias and infiltrating leukocytes of patients with chronic inflammation. The basal level of HO expression in the skin may serve as a first protective environment against acute oxidative and inflammatory insults.
- decompensated type 2 diabetes is associated with increased NADPH oxidase subunit p22(phox) and hemeoxygenase-1 gene expressions in circulating monocytes
- antiproliferative effect of the HO-1 pathway in airway smooth muscle in vitro and in vivo through a bilirubin-mediated redox modulation of phosphorylation of ERK1/2
- These results demonstrate that heme oxygenase-1 operates through distinct molecular mechanisms to confer cytoprotection in the hypoxic and the LPS models of inflammation.
- Data suggest that heme oxygenase-1 gene overexpression may be related to decrease in blood pressure through reduction of the vasodilator 20-hydroxyeicosatetraenoic acid in the urine.
- Results demonstrate that upregulation of heme oxygenase-1 was able to attenuate pyrrolidinedithiocarbamate (PDTC)-mediated cell proliferation, but was unable to reverse the PDTC-induced decrease in angiogenesis in vascular endothelial cells.
- Results suggest that stimulation or overexpression of heme oxygenase-1 attenuates DNA damage caused by exposure to angiotensin II.
- Data suggest that heme oxygenase-1 may be involved in intestinal cell cycle progression.
- heme oxygenase activity up-regulates VEGF production and augments the capability of endothelial cells to respond to exogenous stimulation
- polymorphism of the HO-1 gene is associated with the strength of antiapoptotic effects of HO-1, resulting in an association with susceptibility to oxidative stress-mediated diseases.
- polymorphic (GT)n repeats in the promoter region are not related to neonatal hyperbilirubinemia
- heme oxygenase 1 is induced by P4502E1 through ERK MAPK pathway
- Elucidation of an internal enhancer element regulating induction of this enzyme
- Elucidation of the molecular mechanisms which control HO-1 gene expression will allow us to develop therapeutic strategies to enhance the cytoprotective potential of HO-1 in atherosclerosis.
- Data show that human CD4(+)CD25(+) regulatory T cells constitutively express heme oxygenase-1 (HO-1) and that HO-1 inhibits Jurkat T cell proliferation.
- induction by endogenous nitric oxide
- we report the D140A mutant crystal structure in the Fe(III) and Fe(II) redox states as well as the Fe(II)-NO complex as a model for the Fe(II)-oxy complex.
- there is differential regulation of HO-1 gene expression in parenchymal and non-parenchymal human liver cells
- The AA genotype of HMOX-1 is associated with an increased incidence of hypertension in women
- Heme oxygenase-1 is an antifibrogenic protein in human hepatic myofibroblasts.
- HO-1 has a role in preventing cellular injury via antioxidant mechanisms with aspirin
- Inducibility of HO-1 in G(0)/G(1) phase is essential and probably regulated by a complex system involving oxygen species to assure controlled cell growth
- Heme oxygenase-1 expression attenuates glucose-mediated cell growth arrest and apoptosis in vascular endothelium.
- Basal expression of both HSP72 and HO-1 mRNA were lower (P < 0.05) by 33 and 55%, respectively, when comparing diabetic patients with age-matched and young control subjects
- Induction of HO-1 by hemin results in inhibition of proinflammatory response of endothelial cells, as evidenced by inhibition of IL-8 production without affecting PGI(2) production.
- Collectively, these results indicate that HO-1 is an important protective factor for kidney tissue, in particular, renal tubular epithelial cells.
- Exogenously applied bilirubin and carbon monoxide mimicked the inhibitory effect of heme oxygenase-1 on the chemotactic response
- identified signal pathways and a cAMP-responsive element and a Maf recognition element involved in oxidized phospholipid-mediated HO-1 induction
- This review reaffirms current problems in the biological aspects of HO-1 and suggests an anti-atherogenic role for the enzyme.
- Right ventricle of patients undergoing congenital cardiac surgery differentially expresses haem oxygenase-1 and heat shock protein 70 genes
- regulation of HO expression in the human placenta is a complex process that depends, at least in part, on local glucose and oxygen concentrations.
- These findings identify an array of gene responses to overexpression of human heme oxygenase (HO)-1 and elucidate new aspects of human HO-1 signaling involved in cell growth.
- how HO-1 and WAF1/Cip1 were regulated in two gastric cancer cell lines
- NMR investigation of the solution structure of substrate-free human heme oxygenase
- heme oxygenase-1 has a role in regulating bilirubin and HDL levels but not in coronary artery disease
- We conclude that induction of HO-1 by 15d-PGJ(2) results in augmentation of VEGF synthesis in normoxia.
- HO-1 mRNA and protein are up-regulated in KSHV-infected cultures. Comparison of oral and cutaneous AIDS-KS tissues with normal tissues revealed that HO-1 mRNA and protein were also up-regulated in vivo
- heme oxygenase-1 and ferritin are possible mediators in the antioxidant action of L-alanine
- ATF2 and HO-1 are regulated and induced by biliverdin reductase
- Recombinant adenovirus-mediated HO-1 overexpression in cultured HUVEC umbilical vein endothelial cells inhibits E-selectin and VCAM-1, but not ICAM-1 expression.
- heme oxygenase-1 gene expression is induced by 15-deoxy-delta 12,14-prostaglandin J2 in a reactive oxygen species-dependent manner in human lymphocytes
- Study of the crystal structure of human HO-1 in complex with biliverdin provides insight into the final step in the heme degradation pathway--the rate-limiting step in HO-1 catalysis, which is product, biliverdin, release.
- The AA genotype of HMOX1 reduced the incidence of ischemic heart disease, possibly due to the expression level of HMOX1.
- An influence of the HO-1 gene promoter polymorphism on kidney allograft function, thus supporting previous studies indicating a protective effect of HO-1 induction in organ transplantation.
- Short GT repeats in the HO-1 gene promoter region confer a reduced risk for cerebrovascular events in individuals with normal plasma lipid levels.
- Overexpression of recombinant human HO-1 in rats brings about a reduction in pressor responsiveness to Ang II, likely due to increased generation of an HO-1 product, presumably CO, with the ability to inhibit vascular reactivity to constrictor stimuli.
- The induction of HO-1 in patients with cystic fibrosis is a cytoprotective event and augmenting its expression is a potential therapy against bacterial injury.
- These results indicate that retinal pigment epithelium cells maintain retinal homeostasis by repressing or inducing the expression of heme oxygenase-1, depending on the microenvironment.
- Upregulation of HO-1 decreases oxidant production and endothelial cell damage and shedding and may attenuate vascular complications in diabetes.
- struct-activity relationship of the enzyme
- heme oxygenase oxidation of 5- and 15-phenylhemes involves an electrophilic oxidation mechanism and stereochemical control of the reaction regiospecificity
- study suggests HO-1 is involved in the inhibitory mechanism of flavonoids on LPS-induced iNOS and NO production.
- decreased expression of HO-1 in hepatocytes from hepatitis C virus-infected patients; expression of HO-1 was also reduced in cell lines that stably express HCV core protein, suggesting that core gene products are able to regulate the expression of HO-1
- oxidative stress and p38 MAPK as two consecutive early signals promoting HO-1 induction in hepatic myofibroblasts
- HO-1 mediates the antiinflammatory and antiproliferative effects of simvastatin in VSMCs.
- Polymorphism in heme oxygenase-1 (HO-1) promoter is related to the risk of oral squamous cell carcinoma occurring on male areca chewers
- Review. Promoter polymorphisms in the HO-1 gene exert functional importance by influencing the level of HO-1 expression in different organ systems.
- Bach-1 has a specific and selective ability to repress expression of hepatic heme oxygenase-1
- HO does not exert a pro-oxidant effect involving an non transferrin bound iron increase and that, on the contrary, it could exert an antioxidant effect in premature infants
- HO-1 protects astrocytes from heme-mediated oxidative injury. Specifically increasing astrocytic HO-1 by gene transfer may have a beneficial effect on hemorrhagic CNS injury.
- HO-1 induction protected human hepatocytes against warm and cold hypoxia.
- A network of water molecules, which provide the required protons to activate the iron-oxy complex of heme-HO-1, is absent in both ferrous-verdoheme and the verdoheme-nitric oxide structure.
- heme oxygenase shows differential NADPH- and ascorbate-dependent heme cleavage by the R183E mutant
- Statins lead to HO-1 promoter activation, transcript and protein accumulation
- HO-1 in the liver of acute liver failure patients was highly up-regulated at both transcriptional and protein levels
- Results provide the first evidence for a role of the survival kinase Akt in the regulation of heme oxygenase-1.
- Hemin induced heme oxygenase-1 provided a cytoprotective effect on apoptotic monocytes, despite caspase-3 up-regulation.
- It is possible that HSF-1 negatively regulates HO-1 gene expression, and that the consensus heat shock element present in the -389 to -362 region mediates HSF-1-induced repression of HO-1 gene expression.
- The heme oxygenase-1 expression is in humans pulmonary epithelial cells.
- Foxp3 induces HO-1 expression and HO-1 engages in Foxp3-mediated immune suppression
- results provide a molecular cascade showing nitric oxide-Heme oxygenase(HO)-1-vascular endothelial growth factor (VEGF)-interleukin-8 sequence in human endothelial cells
- These findings suggest that the large size of a (GT)(n) repeat in the HO-1 gene promoter may be associated with the development of lung adenocarcinoma in Japanese male smokers.
- Fine tuning of previously noted active-site hydrogen-bonding network is critical in determining whether heme oxygenase or peroxidase activity is observed.
- BVR advances the role of HO-1 in cytoprotection and affords cytoprotection independent of heme degradation
- The induction of HO-1 is an adaptive response against oxidative damage elicited by lipid peroxidation and it may be critical in the progression of non-alcoholic fatty liver
- There was increased HMOX1 expression in infarcted rat hearts following human bone marrow mesenchymal cell transplantation.
- The functional promoter repeat polymorphism (GT)(n)has no influence of on the development of heart failure, graft survival, acute rejection, or transplant atherosclerosis.
- HIF-1 activation induces substantial HO-1 expression that is associated with attenuated proinflammatory chemokine production by microvascular endothelium in vitro and in vivo.
- transcriptional induction of HO-1 gene expression by AEBSF is mediated via activation of a PKB, p38 MAPK signaling pathway
- findings suggest that the nitric oxide (NO)/ heme oxygenase-1 (HO-1) system has protumoral effects
- ischemia-reperfusion injury and excessive shear stress secondary to portal hypertension might augment HO-1 expression in the graft liver
- heme oxygenase-1 is induced by exercise in human lymphocytes
- Increased HO-1 expression, mainly in Leydig cells, is considered to protect the cells against oxidative stresses in varicocele testes.
- High HO-1 levels in pancreatic cancer calls may be responsible for their anticancer therapy resistance and may act as an endogenous protection mechanism initiated during carcinogenesis
- Serum levels of heme oxygenase-1 are significantly higher in patients with active hemophagocytic syndrome and adult-onset Still's disease than in sera from patients with other diseases that may cause hyperferritinemia.
- activation of PKC, p38(MAPK), JNK, ERK1/2, and Nrf2 by oxidized LDL in human smooth muscle cells leads to HO-1 induction, constituting an adaptive response against oxidative injury that can be ameliorated by vitamin C
- HO-1 is expressed in carotid atherosclerotic plaques infected by Helicobacter pylori
- alpha-lipoic acid induces HO-1 expression in THP-1 monocytic cells via Nrf2 and p38
- The mechanism of heme oxygenase-1 cytoprotection in hepatocytes involves the generation of carbon monoxide and adenosine triphosphate.
- Expression of HO-1 in G0/G1 cells may be a key player in decreasing cellular heme, associated with increased generation of bilirubin, and in attenuating glucose mediated oxidative stress.
- renal expression of HO-1 is regulated in a segment-specific manner, with HO-1 thereby playing distinct roles in different segments of the nephron to maintain renal functions
- HO-1 negatively regulates osteoclastogenesis, leading to a positive net balance of bone
- short (GT)n alleles represent a genetic risk factor for cerebral malaria
- superoxide secondarily generated from damaged mitochondria, not hydroxyl radicals generated in medium directly by sonication, give rise to intracellular oxidative stress inducing HO-1 expression
- HO-1 induction and activity may modulate the production of extracellular matrix components and suggest a potential role for transforming growth factor-beta-mediated HO-1 induction in attenuating renal fibrosis
- In HO-1 overexpressing cells, VEGF and the prostaglandin transporter were greatly increased while monocyte chemoattractant protein-1 levels were decreased
- oxidation of hemoglobin to methemoglobin by low-density lipoprotein (LDL)-associated lipid hydroperoxide and increased sensitivity of cells of the HO-1-deficient child to stress of oxidized LDL might contribute to the vascular disorders reported earlier
- HO-1/IDO cross-regulation modulates apoptosis and proliferation in rat and human breast cancer cells
- Oral squamous cell carcinoma with lymph node metastasis or advanced stage had significantly higher frequency of HO-1 L allelotypes.
- Glial HO-1 expression in the MCI temporal cortex and hippocampus was significantly greater than in the non-demented group and did not differ from AD values.
- HO-1 is involved in an important protective mechanism against PDT-mediated phototoxicity
- Induction of HO-1 inhibits MCP-1 mRNA expression in U937 cells.
- Heme oxygenase-1 plays a vital role in the inhibition of vaso-occlusion in transgenic sickle mice.
- Curcumin induces HO-1 in human hepatocytes, and may show protective effects in pretreatment during hepatic transplantation.
- key role of down-regulation of Bach1 and up-regulation of heme oxygenase 1 in diminishing cytotoxic effects of hepatitis C virus proteins in human hepatocytes.
- expression of HO-1, but not HO-2, was upregulated within the nasal tissues in allergic rhinitis inflammation, and understanding the induction of HO-1 expression may provide for better management of allergic rhinitis that involves oxidative stress.
- Treatment of keratinocytes with hemin induced HO-1 expression & activity. Involvement of HO-1 in VEGF synthesis was confirmed by inhibition of VEGF expression by SnPPIX, blocker of HO activity & by attenuation of HO-1 mRNA expression with specific siRNA.
- The large size of a (GT)n repeat in the HO-1 gene promoter may be associated with susceptibility to pneumonia in the older Japanese population.
- Microsatellite polymorphism in the heme oxygenase-1 gene promoter is associated with risk for melanoma
- atorvastatin prevents hypoxia-induced inhibition of endothelial nitric oxide synthase expression but does not affect heme oxygenase-1 in human microvascular endothelial cells
- Our results support an antiapoptotic role for HO-1 in Caco-2 cells and provide a mechanism by which overexpression of HO-1 may promote tumor resistance to stress in conditions of limited nutrient supply.
- proton pump inhibitors induce heme oxygenase-1 in gastric and endothelial cells
- The focus of this review is on the importance of the stress-responsive heme oxygenase-1 induction system as a cytoprotective program.
- Data show that beta-carotene, combined with cigarette smoke condensate (TAR), regulates heme oxygenase-1 (HO-1) via its transcriptional factor Bach1 and modulates cell growth.
- The adaptation of HO-1 mRNA expression assay as a biologically relevant indicator of cigarette smoke-induced stress.
- early thrombolysis induced by CO in HO-1-mediated protection against intimal hyperplasia after vascular injury
- anti-inflammatory actions mediated by gliotoxin include HO-1 induction and the subsequent blockade of NF-kappaB-dependent signaling pathways in vitro and in vivo
- HO-1 and Akt exert codependent cytoprotective effects against oxidative stress-induced apoptosis in human aortic smooth muscle cells.
- The antiapoptotic effect of HO-1 in endothelial cells is dependent on the degradation of p38alpha MAP kinase isoform by the 26S proteasome and on the expression of p38beta MAP kinase.
- These results suggest that a long (L) HO-1 gene promoter in heavy smokers is associated with susceptibility to develop airway obstruction.
- In Alzheimer disease brain, alpha(1)-antitrypsin immunoreactivity was augmented and co-distributed with heme oxygenase-1
- These results thus demonstrate that BRG1, through the facilitation of Z-DNA formation and subsequent recruitment of RNA polymerase II, is critical in Nrf2-mediated inducible expression of HO-1.
- up-regulation of HO-1 by non-steroidal anti-inflammatory drugs (NSAIDs) is mediated through NSAID-dependent activation (phosphorylation) of p38 mitogen-activated protein kinase
- nuclear factor (erythroid-derived 2)-like 2-mediated HO-1 overexpression confers resistance to apoptosis induction by EGCG
- Sulforaphane transcriptionally activates the upstream ARE-rich enhancer region, located at -9.0 kb upstream human HO-1 promoter.
- HO-1 and carbon monoxide require endothelial STAT3 for their protective effects, and STAT3 confers endothelial cell protection via both HO-1-dependent and independent mechanisms
- HO-1 expression and activity in endothelial cells are present only in advanced atherosclerosis, whereas VEGF expression is present in early as well as in advanced atherosclerosis and the degree of expression increases with severity of atherosclerosis.
- HO-1 gene overexpression in rat islets by adenovirus transduction can protect cultured islets against recombinant TNF-alpha and cycloheximide-mediated cytotoxicity.
- Inhibition of HO1 by Motexafin gadolinium may contribute to its anticancer activity.
- Bach2 is phosphorylated on S521 via Bcr-Abl signaling thru the phosphatidylinositol-3/S6 kinase pathway,and transcriptionally represses heme oxygenase-1
- lipid peroxidation is a significant cause of NO-induced necrosis in human lung epithelial cells, but increased NO survival of rat cells is due to decreased lipid peroxidation mediated by HO-1-generated biliverdin or bilirubin
- heme oxygenase-1 is down regulated by heme oxygenase-2.
- The effect of Bach1 and Nrf2 on heme oxygenase 1 expression via cobalt protoporphyrin in human liver cells is reported.
- We demonstrate the functional compartmentalization of heme oxygenase-1 in the mitochondria of lung epithelial cells, and its potential role in defense against mitochondria-mediated cell death during CSE exposure.
- symptomatic plaques show a more pronounced induction of CD163 and HO-1 in response to plaque hemorrhages.
- Genetic polymorphisms in HOX-1 and mEPH genes are associated with the development of COPD in Southwest China
- JunB and JunD contribute opposing effects; JunB activated whereas JunD repressed heme oxygenase-1 expression in human renal epithelial cells
- The basal levels of Hsp32 (HMOX1), Hsp70 and Hsp90 increased significantly with age in controls. Higher levels of Hsp32, Hsp70 and Hsp90 were noticed in patients with inflammation.
- Expression of heme oxygenase 1 (HO-1) correlated with CD4+ CD25+ FoxP3+ (Treg)infiltration. HO-1 expressing Treg accumulate during glioma progression. HO-1 mRNA expression is linked to the induction of Foxp3 in CD4+ CD25+ glioma infiltrating Treg.
- Results indicate that stimulation of heme oxygenase-1 expression by hypericin-PDT is a cytoprotective mechanism governed by the p38(MAPK) and PI3K pathways.
- The main catabolic process that degrades heme, the heme oxygenase (HO) system, is reviewed, and evidence for the protective effects of HO-1 against acute and chronic heme/heme protein-induced renal injury is summarized. [REVIEW]
- HSF1 is directly involved in the regulation of HO-1 with an anti-oxidative role
- Both vitreous and TGF-beta signals increased HO-1 expression in retinal pigment epithelial cells via reactive oxygen species.
- Increased HO-1 in premature senescence of fetal lung fibroblasts induced by both tert-butylhydroperoxide and ethanol.
- As highlighted in this review, HO-1 can be a potent protector; in other circumstances, a seemingly disinterested bystander; and in still others, a pernicious perpetrator of cellular damage.
- No evidence of any protective effect for the S-allele of the HO-1 gene promoter polymorphism on graft or recipient survival in renal transplantation.
- The findings of this study does not support a clinically relevant association of the HO-1 promoter polymorphism with restenosis and ischaemic events after coronary stenting.
- HO-1 expression is transcriptionally regulated by PPAR-alpha or PPAR-gamma.
- We have identified novel nonclassical mediators of the SREBP-1 response, including HMOX1, supporting the hypothesis that SREBP-1 regulates stress response and signaling genes.
- These results suggest that HO-1 transgene expression regulated by an enhanced GFAP promoter selectively increases HO-1 expression in astrocytes, and is cytoprotective
- Inhibition of HO-1 significantly increases T cell proliferation against human embryonic stem cells
- The findings suggest that the long (GT)n repeat of HO-1 was associated with a greater frequency of gastric adenocarcinoma.
- In Parkinson's disease brain, overexpression of HO-1 in nigral astroglia and accompanying iron liberation may facilitate bioactivation of dopamine to neurotoxic free radical intermediates and predispose nearby neuronal constituents to oxidative damage.
- BAX inhibitor 1 functions involve the expression of heme oxygenase-1 (HO-1) through nuclear factor erythroid 2-related factor 2.
- Induction of heme oxygenase-1 in renovascular hypertension is associated with inhibition of apoptosis.
- the capacity to upregulate HO-1 expression may be determined, at least in part, by genetics, and reduced ability to induce HO-1 may be involved in the mechanism of coronary atherosclerosis
- study shows HO-1 expression rate of 41.8% in colorectal cancer & 36.8% in colon adenoma; expression associated with lower rate of lymphatic invasion & tendency of fewer lymph node metastases; patients with HO-1 expressing colon cancer had better survival
- The molecular regulation of heme oxygenase-1 by transforming growth factor-beta1 in human renal proximal tubular cells is reported.
- Inhibition of HO-1 function or expression further increases the proproliferative capacity of pulmonary artery smooth muscle cells.
- Curcumin has an ability to induce HO-1 expression, presumably through Nrf2-dependent ARE activation, in rat VSMCs and HASMCs
- Suppression of antigen-presenting cells may represent a main anti-inflammatory mechanism of HO-1
- HO-1 can regulate the expression of the anti-angiogenic CXCL-10 and may alter a critical balance between angiogenic vs. anti-angiogenic factors that are important to maintain renal microvasculature during injury.
- Isothiocyanates activate antioxidant response element(ARE)-mediated HO-1 gene transcription through Nrf2/ARE signaling pathway.
- Heme oxygenase-1 (HO-1) gene transcript in the donor hearts was up-regulated with D-4F treatment, and HO-1 blockade partially reversed the beneficial effects of D-4F.
- These data suggest that HCV core protein may contribute to hepatocellular injury by increasing both steady-state levels of prooxidants and the susceptibility of hepatocytes to damage by impairing their response to other sources of oxidative stress.
- potentially higher levels of iron-generated oxidative stress related gene alleles may be at increased risk of breast cancer
- carbon monoxide renders endothelial cells resistant to stress by upregulating Nrf2-dependent HO-1 expression via PERK activation
- Anticipation of subsequent demanding exercise increases the expression of haem oxygenase-1 mRNA in human lymphocytes.
- stress-induced HO-1 initially plays a protective role, while its chronic upregulation, might contribute to oligodendroglial cell death rather than providing protection
- Targeting endothelial cells with HO-1 using VE-cadherin promoter attenuates hyperglycemia-mediated cell injury and apoptosis.
- heme oxygenase-1 increases in human lymphocytes after exercise
- Continuously elevated HO-1-activity protects EC from oxidative stress but inhibits Akt-mediated proliferation and eNOS-expression. This inhibitory feedback mechanism could be a limitation of HO-1 as a target for the treatment of vascular disease.
- hHO-1 has the potential to incorporate into phospholipid membranes, which can be reconstituted at known concentrations, in combination with other endoplasmic reticulum resident enzymes
- HO-1 showed a pronounced antiviral activity in hepatitis B virus infection.
- micro-RNA-122 (miR-122) plays an important role in the regulation of hepacvirus replication and heme oxygenase-1/Bach1 expression in hepatocytes.
- Atorvastatin-mediated HO-1 upregulation, and its associated antioxidant effect, are KLF2-dependent.
- These results suggest that HO-1 modulates the inflammatory pain pathways. Hence, the development of drugs that could raise peripheral HO-1 could be relevant in inflammatory pain treatment.
- The results suggest that high levels of beta-carotene might counterbalance the effects on FEV1 decline determined by heme oxygenase-1 gene promoter polymorphism.
- Microsatellite polymorphism in the heme oxygenase-1 gene promoter is associated with iron status in persons with type 2 diabetes mellitus.
- A significant association was found between oxidative stress GSTM1 deletion and the HMOX-1 long repeat and heart rate variation in response to particulate air pollution.
- Based on these results, we conclude that HO activity is involved in the regulation of p53 expression in a ROS-independent mechanism.
- the functional HO-1 promoter polymorphism does not influence renal survival in CKD due to ADPKD or IgAN
- Functional promoter variants in CAT and HMOX-1 showed ethnicity-specific associations with new-onset asthma.
- HO-1 (GT)(n) microsatellite is a new genetic marker involved in rheumatoid arthritis genetics.
- Glucosamine sulfate up-regulated expression of HO-1 in human osteoarthritis chondrocytes.
- HO-1 genotype mediates graft survival after liver transplantation
- Thus, PGD(2) may contribute to the maintenance of heme homeostasis in the brain by inducing HO-1 expression.
- REVIEW: overview of the role of heme oxygenase-1 and carbon monoxide in angiogenesis, and associated disorders.
- Patients with a first venous thromboembolism and long GT-repeat alleles in HMOX1 have an increased risk of recurrence.
- a novel mechanism by which TNF-induced cell death is inhibited in AML cells through the induction of HO-1, via Nrf2 activation.
- plays a principal role in the protective response to nicotine in oral cancer and immortalized keratinocytes
- The expression of haem oxygenase-1 is decreased in macrophages of idiopathic pulmonary fibrosis patients compared with those with granulomatous lung disorders
- Upregulated TLR4 is associated with HO-1 reduction in peripheral blood monocytes from patients with Behcet's disease, leading to augmented inflammatory responses.
- Higher levels of HMOX1 is associated with delayed graft function.
- HO-1 was correlated with the degree of epithelial dysplasia. Oral squamous cell carcinoma also showed elevated expression of HO-1, but this level was not higher than in severe OED or carcinoma in situ.
- human blood ozonation induces a remarkable upregulation of heme oxygenase-1 and heat stress protein-70
- HO-1 upregulation by SAM was causally related to a decrease in NADPH-mediated production of oxygen radicals. Our results demonstrate that the HO-1/ferritin-system is a novel target of the antioxidant compound S-adenosylmethionine.
- Increased decidual and serum HMOX1 levels, together with altered decidual expression of some stress-related genes in cases, support the role of oxidative stress and excessive maternal inflammatory response in the pathogenesis of PE.
- Presence of short GTn-allele was associated with a lower tumor recurrence rate and better relapse-free survival in OSCC patients. HMOX-1 promoter polymorphism might be considered as a potential prognostic marker in OSCC patients.
- The expression level of HO-1 gene is a marker for Cr(VI)-induced cell stress leading to cytotoxicity.
- Inhibition of plasminogen activator inhibitor-1 expression in vascular smooth muscle cells by protoporphyrins through a heme oxygenase-independent mechanism.
- Overexpression of HO-1 releasing molecules may provide a therapeutic strategy to improve cell viability during neural differentiation in applications that use stem cell technology.
- Enterohemorrhagic Escherichia coli-induced heme oxygenase-1 in human epithelial cells is a critical modulator of the innate immune response.
- chlorophyllin exerts antioxidant effect by inducing HO-1 and NQO1 expression mediated by PI3K/Akt and Nrf2
- Polymorphism in the HO-1 gene promoter is correlated with susceptibility to coronary artery disease in diabetic patients.
- Improved renal function after kidney transplantation is associated with heme oxygenase-1 polymorphism
- association between cardiac response to submaximal exercise and HMOX-1 genotype
- beneficial role of HO-1 in blocking tumor invasion was first identified in this study.
- genetic polymorphisms of HO-1 and iNOS modulate individual susceptibility to gastric cancer risk.
- Down-regulation of HO-1 expression in neutrophils from hypertensive subjects may be exerted through the inhibition of NOS2 expression.
- HO-1 protein turnover is regulated by the ubiquitin-proteasome system through the endoplasmic reticulum-associated degradation pathway
- Loss of BACH1 function in human keratinocytes results almost exclusively in HMOX1 induction, suggesting that BACH1 may function as a rheostat regulating levels of intracellular free heme.
- REVIEW of role of HO-1 in protecting against vascular injury
- specific knockdown of HO-1 might represent a novel therapeutic approach in hepatocellular carcinoma therapy.
- HO-1 protects endothelial cells from apoptosis, is involved in blood-vessel relaxation regulating vascular tone, attenuates inflammatory response in the vessel wall, & participates in blood-vessel formation via angiogenesis & vasculogenesis. Review.
- HO-1 levels were increased in sera and skin lesions of patients with atopic dermatitis and were associated with disease severity
- These results demonstrate for the first time that epigallocatechin-induced HO-1 expression occurs via PKCdelta and Nrf2.
- Significantly different distribution of the HO-1 genotype was found in subjects with different-stage urothelial carcinomas; however, it was not related to the NAD(P)H:quinone oxidoreductase 1 genotype.
- CO, a product of heme catabolism by HO-1, directly inhibits alpha1C subunit of the cardiac L-type Ca2+ channel
- No association was detected between the TGFB1, IL10, TP53, and HMOX1 genes and DGF. The G allele of the TNF polymorphism rs3093662 was associated with DGF in an adjusted analysis.
- mRNA expressions of Hsp70, Hsp32 and Bax significantly increased in mononuclear blood cells after marathon running, whereas Hsp27 and Bad mRNA expression levels showed no significant changes.
- Heme oxygenase-1 expression decreased LPS-stimulated secretion of MCP-1, IL-6, IL-10, and TNF-alpha at both 4 and 24 h in murine and human macrophages
- Glutathione-induced increase in HO-1 may help protect against cigarette smoke-induced inflammation and/or cell death.
- Results suggest that human heme oxygenase-1-modified mesenchymal stem cells prevent myocardial cell injury via secretion of paracrine-acting mediators.
- These studies demonstrated an interdependence of autophagic and apoptogenic signaling in cigarette smoke extract -induced cell death, and their coordinated downregulation by HO-1.
- potentially autoprotective and autodefensive role in several pathophysiological states including acute coronary syndromes and stroke
- HO-1 has a significant protective effect against airway mucus hypersecretion in animals and humans exposed to cigarette smoke.
- Results suggest that the signals evoked by hypoxia and after ethyl-3,4-dihydroxybenzoate treatment differentially regulate HO-1 mRNA expression through HIF-1alpha-independent mechanisms.
- donor polymorphism leading to high expression of HO-1 (<30 GT repeats) on stress signals is associated with reduced overall survival in hematopoietic stem cell transplantation recipients
- Heme oxygenase enzyme (HO-1) activity in the human seminal plasma is related to spermatogenesis and sperm-motility processes.
- Subjects carrying the HO-1 genotype had a more than 6.5-time higher risk of developing Alzheimer's disease than subjects without these risk genotypes
- HO-1 is a negative regulator of trophoblast motility acting via up-regulation of PPARgamma.
- YC-1 stimulates the expression of HMOX1 in vascular smooth muscle cells.
- Increased heme oxygenase 1 expression is associated with multiple sclerosis lesions.
- PGD(2) induces HO-1 mRNA expression through DP2 receptor, linking the PGD(2)-DP2 signaling with heme homeostasis.
- The aim of this study was to determine whether the (GT)n-repeat length within the HMOX1 promoter region is associated with RA disease severity and radiographic joint damage.
- LPS induces NQO1 and HO-1 expression in human monocytes via Nrf2 to modulate their inflammatory responsiveness
- HO-1 negatively regulates thrombopoiesis by inhibiting reactive oxygen species.
- Induction of prostacyclin by steady laminar shear stress suppresses tumor necrosis factor-alpha biosynthesis via heme oxygenase-1 in human endothelial cells.
- HO-1 gene promoter length polymorphism is related to the renal impairment of IgA nephropathy at the time of diagnosis
