scholarly journals Paradoxical enhancement of oxidative cell injury by overexpression of heme oxygenase-1 in an anchorage-dependent cell ECV304

2004 ◽  
Vol 93 (3) ◽  
pp. 552-562 ◽  
Author(s):  
Keiko Maruhashi ◽  
Yoshihito Kasahara ◽  
Kunio Ohta ◽  
Taizo Wada ◽  
Kazuhide Ohta ◽  
...  
Keyword(s):  
Heme Oxygenase ◽  
Cell Injury ◽  
Heme Oxygenase 1 ◽  
Dependent Cell

scholarly journals Protective Effect of Heme Oxygenase-1 on High Glucose-Induced Pancreatic β-Cell Injury

2011 ◽  
Vol 35 (5) ◽  
pp. 469 ◽  
Author(s):  
Eun-Mi Lee ◽  
Young-Eun Lee ◽  
Esder Lee ◽  
Gyeong Ryul Ryu ◽  
Seung-Hyun Ko ◽  
...  
Keyword(s):  
Protective Effect ◽  
Heme Oxygenase ◽  
High Glucose ◽  
Cell Injury ◽  
Heme Oxygenase 1 ◽  
Pancreatic Β Cell ◽  
Β Cell

scholarly journals Oxidative stress causes enhanced endothelial cell injury in human heme oxygenase-1 deficiency

1999 ◽  
Vol 103 (1) ◽  
pp. 129-135 ◽  
Author(s):  
Akihiro Yachie ◽  
Yo Niida ◽  
Taizo Wada ◽  
Noboru Igarashi ◽  
Hisashi Kaneda ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cell ◽  
Heme Oxygenase ◽  
Cell Injury ◽  
Heme Oxygenase 1 ◽  
Endothelial Cell Injury

scholarly journals Heme oxygenase-1 induction contributes to renoprotection by G-CSF during rhabdomyolysis-associated acute kidney injury

2011 ◽  
Vol 301 (1) ◽  
pp. F162-F170 ◽  
Author(s):  
Qingqing Wei ◽  
William D. Hill ◽  
Yunchao Su ◽  
Shuang Huang ◽  
Zheng Dong
Keyword(s):  
Acute Kidney Injury ◽  
Heme Oxygenase ◽  
Cell Injury ◽  
Kidney Injury ◽  
Heme Oxygenase 1 ◽  
Protective Effects ◽  
Tubular Cells ◽  
Renal Tubular Cells

Granulocyte colony-stimulating factor (G-CSF) is renoprotective during acute kidney injury (AKI) induced by ischemia and cisplatin nephrotoxicity; however, the underlying mechanism is not entirely clear. Rhabdomyolysis is another important clinical cause of AKI, due to the release of nephrotoxins (e.g., heme) from disrupted muscles. The current study has determined the effects of G-CSF on rhabdomyolysis-associated AKI using in vivo and in vitro models. In C57BL/6 mice, intramuscular injection of glycerol induced AKI, which was partially prevented by G-CSF pretreatment. Consistently, glycerol-induced renal tissue damage was ameliorated by G-CSF. In addition, animal survival following the glycerol injection was improved from ∼30 to ∼70% by G-CSF. In cultured renal tubular cells, hemin-induced apoptosis was also suppressed by G-CSF. Interestingly, G-CSF induced heme oxygenase-1 (HO-1, a critical enzyme for heme/hemin degradation and detoxification) in both cultured tubular cells and mouse kidneys. Blockade of HO-1 with protoporphyrin IX zinc(II) (ZnPP) could largely diminish the protective effects of G-CSF. Together, these results demonstrated the renoprotective effects of G-CSF in rhabdomyolysis-associated AKI. Notably, G-CSF may directly protect against tubular cell injury under the disease condition by inducing HO-1.

Role of heme oxygenase-1 in endotoxemic acute renal failure

2005 ◽  
Vol 289 (6) ◽  
pp. F1382-F1385 ◽  
Author(s):  
Brian Poole ◽  
Wei Wang ◽  
Yung-Chang Chen ◽  
Einath Zolty ◽  
Sandor Falk ◽  
...  
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Acute Renal Failure ◽  
Heme Oxygenase ◽  
Cell Injury ◽  
Heme Oxygenase 1 ◽  
Zinc Protoporphyrin ◽  
Renal Protection ◽  
Renal Vasoconstriction

The pathogenesis of septic acute renal failure (ARF) involves systemic vasodilation with compensatory upregulation of vasoconstrictors. This can lead to renal vasoconstriction and ARF. Heme oxygenase (HO) is the rate-limiting step in heme metabolism and produces carbon monoxide (CO) and biliverdin. HO-1 is an inducible form of the enzyme and is expressed in response to cell injury. It was hypothesized in endotoxemia, induction of HO-1 would lead to increased production of the vasodilator CO, lower blood pressure, and decrease renal function. The role of HO-1 was therefore examined in a mouse model of endotoxemia. One group of mice received LPS alone and were compared with mice that received LPS in addition to an inhibitor of HO-1, zinc protoporphyrin (ZnPP). Treatment of mice with LPS resulted in significant increases in the protein expression of HO-1 compared with controls treated with vehicle. Immunohistochemical analysis localized this upregulation to both the proximal and distal tubules as well as the vasculature. Hemodynamic studies were performed during endotoxemia and the mean arterial pressure (MAP) was found to be significantly higher in the HO-1 inhibitor-treated compared with vehicle-treated mice (78 ± 3 vs. 64 ± 2 mmHg, P < 0.01). It was found that the inhibitor group had higher renal blood flows (RBF) also during endotoxemia (1.8 ± 0.2 vs. 0.68 ± 0.1 ml/min, P < 0.01). Furthermore, when renal vascular resistance (RVR) was calculated, there was a significant decrease in RVR in the inhibitor group (43.5 ± 3.4 vs. 95.9 ± 11.3 mmHg·ml−1·min−1, P < 0.01). In concert with the hemodynamic data, glomerular filtration rate (GFR), as measured by inulin clearance, was higher in the HO inhibitor compared with the vehicle controls during endotoxemia (111.5 ± 19.5 vs. 66.0 ± 3.5 μl/min, P < 0.05). In summary, during endotoxemia ARF, inhibiting HO-1 with ZnPP resulted in the protection of renal function. The renal protection was associated with significantly improved systemic hemodynamics, less renal vasoconstriction, and a higher GFR.

scholarly journals Donor Heme Oxygenase-1 Promoter Gene Polymorphism Predicts Survival after Unrelated Bone Marrow Transplantation for High-Risk Patients

Cancers ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 424
Author(s):  
Tomohiro Horio ◽  
Eriko Morishita ◽  
Shohei Mizuno ◽  
Kaori Uchino ◽  
Ichiro Hanamura ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Transplantation ◽  
High Risk ◽  
Heme Oxygenase ◽  
Marrow Transplantation ◽  
Cell Injury ◽  
Disease Free Survival ◽  
Heme Oxygenase 1 ◽  
Intracellular Enzyme ◽  
Promoter Gene

Heme oxygenase-1 (HO-1), an intracellular enzyme that catalyzes the degradation of heme into biliverdin, free iron, and carbon monoxide, exerts anti-inflammatory and cytoprotective effects against endothelial cell injury. The HO-1 promoter gene has one important single-nucleotide polymorphism (SNP) rs2071746 (-413A>T) that is functional, and the A allele has been reported to be associated with higher HO-1 expression levels than the T allele. We investigated the influence of the HO-1 rs2071746 SNP on the transplant outcomes in 593 patients with hematological malignancies undergoing unrelated, human leukocyte antigen (HLA)-matched, T-cell-replete bone marrow transplantation (BMT) through the Japan Donor Marrow Program. In patients with high-risk diseases, the donor A/A or A/T genotype was associated with better 5 year overall survival (35% vs. 25%; p = 0.03) and 5 year disease-free survival (35% vs. 22%; p = 0.0072), compared to the donor T/T genotype. These effects were not observed in patients with low-risk diseases. The current findings therefore indicate that HO-1 rs2071746 genotyping could be useful for selecting donors and tailoring transplant strategies for patients with high-risk hematologic malignancies.

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