دورية أكاديمية

Localization of phosphorylated αB-crystallin to heart mitochondria during ischemia-reperfusion.

التفاصيل البيبلوغرافية
العنوان: Localization of phosphorylated αB-crystallin to heart mitochondria during ischemia-reperfusion.
المؤلفون: Jin, J.-K., Whittaker, R., Glassy, M. S., Barlow, S. B., Gottlieb, R. A., Glembotski, C. C.
المصدر: American Journal of Physiology: Heart & Circulatory Physiology; Jan2008, Vol. 294 Issue 1, pH337-H344, 8p, 7 Graphs
مصطلحات موضوعية: MITOCHONDRIA, HEART, HEART cells, ISCHEMIA, REPERFUSION, HEAT shock proteins, MITOCHONDRIAL membranes, HYGIENE
مستخلص: The cytosolic small heat shock protein αB-crystallin (aBC) is a molecular chaper- one expressed in large quantities in the heart, where it protects from stresses such as ischemia-reperfusion (I/R). Upon I/R, p38 MAP kinase activation leads to phosphorylation of αBC on Ser59 (P-αBC- S59), which increases its protective ability. αBC confers protection, in part, by interacting with and affecting the functions of key components in stressed cells. We investigated the hypothesis that protection from I/R damage in the heart by P-αBC-S59 can be mediated by localization to mitochondria. We found that P-αBC-S59 localized to mitochondria isolated from untreated mouse hearts and that this localization increased more than threefold when the hearts were subjected to ex vivo I/R. Mitochondrial P-αBC-S59 decreased when hearts were treated with the p38 inhibitor SB-202 190. Moreover, SB-202190-treated hearts exhibited more tissue damage and less functional recovery upon reperfusion than controls. I/R activates mitochondrial permeability transition (MPT) pore opening, which increases cell damage. We found that mitochondria incubated with a recombinant mutant form of aBC that mimics P-αBC-S59 exhibited decreased calcium-induced MPT pore opening. These results indicate that mitochondria may be among the key components in stressed cells with which P-αBC-S59 interacts and that this localization may protect the myocardium, in part, by modulating MPT pore opening and, thus, reducing I/R injury. [ABSTRACT FROM AUTHOR]
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قاعدة البيانات: Complementary Index
الوصف
تدمد:03636135
DOI:10.1152/ajpheart.00881.2007