| First Author | Kim J | Year | 2017 |
| Journal | Biochem Biophys Res Commun | Volume | 485 |
| Issue | 4 | Pages | 807-813 |
| PubMed ID | 28257842 | Mgi Jnum | J:250979 |
| Mgi Id | MGI:6102679 | Doi | 10.1016/j.bbrc.2017.02.136 |
| Citation | Kim J, et al. (2017) PICOT alleviates myocardial ischemia-reperfusion injury by reducing intracellular levels of reactive oxygen species. Biochem Biophys Res Commun 485(4):807-813 |
| abstractText | Excessive generation of reactive oxygen species (ROS) is one of the main causes of myocardial ischemia-reperfusion (I/R) injury. In this study, we investigated the role of protein kinase C-interacting cousin of thioredoxin (PICOT; Grx3) during myocardial I/R using PICOT transgenic (TG) and knockdown (KD) mice. Infarction and apoptosis were attenuated in PICOT TG mice but exacerbated in PICOT KD mice upon I/R. In parallel, I/R-induced generation of ROS was attenuated in PICOT TG mice but exacerbated in PICOT KD mice. Angiotensin II (AngII)-mediated increases in ROS and free iron levels were also attenuated in cardiomyocytes isolated from PICOT TG mice but exacerbated in cardiomyocytes from PICOT KD mice. Accordingly, H2O2-mediated cell death was attenuated in cardiomyocytes isolated from PICOT TG mice but exacerbated in cardiomyocytes from PICOT KD mice. Taken together, these data show that PICOT alleviates myocardial I/R injury by regulating intracellular ROS and free iron levels. We suggest that PICOT presents a novel therapeutic strategy for myocardial I/R injury. |
