| First Author | Qiao Y | Year | 2020 |
| Journal | Biochem Biophys Res Commun | Volume | 521 |
| Issue | 4 | Pages | 1095-1100 |
| PubMed ID | 31733834 | Mgi Jnum | J:291712 |
| Mgi Id | MGI:6445422 | Doi | 10.1016/j.bbrc.2019.11.053 |
| Citation | Qiao Y, et al. (2020) Hepatocellular HO-1 mediated iNOS-induced hepatoprotection against liver ischemia reperfusion injury. Biochem Biophys Res Commun 521(4):1095-1100 |
| abstractText | Hepatocyte-derived inducible nitric oxide synthase (iNOS) was proved to impart protection against liver ischemia reperfusion (I/R) injury in our prior analysis. However, the mechanism for this hepatoprotection remains incompletely understood. Bone marrow chimeric mice were generated using expression of iNOS in a hepatocyte-selective manner against an iNOS-knockout background. The function of heme oxygenase 1 (HO-1) in iNOS-stimulated hepatoprotection and the molecular mechanisms were explored in vitro and in vivo, respectively. Hepatocyte-derived iNOS conferred protection from I/R injury and anoxia/reoxygenation stimulation. Mechanistically, iNOS activated nuclear factor erythroid 2-related factor 2 (Nrf-2) and subsequently, stimulated the transcription of HO-1. Results from our study led to the conclusion that HO-1 is another potent mediator of iNOS-mediated protection after liver I/R. |
