Myocardial protection from ischemia/reperfusion injury by endogenous and exogenous HGF
AUTOR(ES)
Nakamura, Teruya
FONTE
American Society for Clinical Investigation
RESUMO
Using a rat model of ischemia/reperfusion injury, we demonstrate here that HGF is cardioprotective due to its antiapoptotic effect on cardiomyocytes. Following transient myocardial ischemia and reperfusion, c-Met/HGF receptor expression rapidly increased in the ischemic myocardium, an event accompanied by a dramatic increase in plasma HGF levels in the infarcted rats. When endogenous HGF was neutralized with a specific antibody, the number of myocyte cell deaths increased markedly, the infarct area expanded, and the mortality increased to 50%, as compared with a control group in which there was no mortality. Plasma from the myocardial infarcted rats had cardioprotective effects on primary cultured cardiomyocytes, but these effects were significantly diminished by neutralizing HGF. In contrast, recombinant HGF administration reduced the size of infarct area and improved cardiac function by suppressing apoptosis in cardiomyocytes. HGF rapidly augmented Bcl-xL expression in injured cardiomyocytes both in vitro and in vivo. As apoptosis of cardiomyocytes is one of the major contributors to the pathogenesis in subjects with ischemia/reperfusion injury, prevention of apoptosis may prove to be a reasonable therapeutic strategy. Supplements of HGF, an endogenous cardioprotective factor, may be found clinically suitable in treating subjects with myocardial infarction.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=387252Documentos Relacionados
- Long non-coding RNA-ROR aggravates myocardial ischemia/reperfusion injury
- von Willebrand factor, exercise, and ischemia/reperfusion injury.
- Interleukin 1 pretreatment decreases ischemia/reperfusion injury.
- Effect of Simulated Geomagnetic Activity on Myocardial Ischemia/Reperfusion Injury in Rats
- Grape seed protects cholestatic rats liver from ischemia/reperfusion injury