| First Author | Otsu K | Year | 2003 |
| Journal | Biochem Biophys Res Commun | Volume | 302 |
| Issue | 1 | Pages | 56-60 |
| PubMed ID | 12593847 | Mgi Jnum | J:82448 |
| Mgi Id | MGI:2653008 | Doi | 10.1016/s0006-291x(03)00096-2 |
| Citation | Otsu K, et al. (2003) Disruption of a single copy of the p38alpha MAP kinase gene leads to cardioprotection against ischemia-reperfusion. Biochem Biophys Res Commun 302(1):56-60 |
| abstractText | The p38 mitogen-activated protein kinase (p38) is activated in the heart during ischemia-reperfusion. However, it is not clear whether the activation of p38 is the protective response or the kinase mediates the cellular damage by ischemia-reperfusion. We examined the role of p38alpha in ischemia-reperfusion injury by studying p38alpha(+/-) mice. The p38alpha protein level in the p38alpha(+/-) heart was 50+/-8.7% compared with that in the p38alpha(+/+) heart. Upon reperfusion following ischemia for 25min, p38alpha activity was transiently increased. The maximum level of p38 activity in p38alpha(+/-) was 60+/-10.5% compared with that in p38alpha(+/+). In the p38alpha(+/+) heart, 25min ischemia and 2h reperfusion resulted in necrotic injury (37.1+/-2.7% of the area at risk), whereas infarct size was drastically reduced to 7.2+/-0.7% in the p38alpha(+/-) heart. These suggested that p38alpha plays a pivotal role in the signal transduction pathway mediating myocardial cell death caused by ischemia-reperfusion. |
