Translocation of deltaPKC to mitochondria during cardiac reperfusion enhances superoxide anion production and induces loss in mitochondrial function.

Abstract:

:Activation of the delta-isoform of protein kinase C (deltaPKC) by certain conditions of oxidative stress results in translocation of the kinase to the mitochondria leading to release of cytochrome c and the induction of apoptosis. In the current study, the effects of myocardial reperfusion-induced deltaPKC translocation on mitochondrial function were assessed. Mitochondria isolated from hearts that had undergone ischemia (30 min) followed by reperfusion (15 min) exhibited a significant increase in the rate of superoxide anion (O(2)(-)) generation. This was associated with the translocation of deltaPKC to the mitochondria within the first 5 min of reperfusion. deltaPKC translocation occurred exclusively during reperfusion and could be mimicked by infusion of intact hearts with H(2)O(2) suggesting redox-dependent activation during reperfusion. Infusion of a peptide inhibitor (deltaV(1-1)) specific to the delta-isoform of PKC significantly reduced reperfusion-induced increases in mitochondrial O(2)(-) generation. Finally, the decline in mitochondrial respiratory activity evident upon prolonged reperfusion (120min) was completely prevented by inhibition of deltaPKC translocation. Thus, deltaPKC represents a cytosolic redox-sensitive molecule that plays an important role in amplification of O(2)(-) production and subsequent declines in mitochondrial function during reperfusion.

journal_name

Arch Biochem Biophys

authors

Churchill EN,Szweda LI

doi

10.1016/j.abb.2005.05.007

subject

Has Abstract

pub_date

2005-07-15 00:00:00

pages

194-9

issue

2

eissn

0003-9861

issn

1096-0384

pii

S0003-9861(05)00191-8

journal_volume

439

pub_type

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