Translocation of protein kinase C-alpha,delta and epsilon isoforms in ischemic rat heart

被引:85
作者
Yoshida, K
Hirata, T
Akita, Y
Mizukami, Y
Yamaguchi, K
Sorimachi, Y
Ishihara, T
Kawashiama, S
机构
[1] YAMAGUCHI UNIV, SCH MED, DEPT PATHOL, UBE, YAMAGUCHI 755, JAPAN
[2] YAMAGUCHI UNIV, SCH MED, ANIM CTR, UBE, YAMAGUCHI 755, JAPAN
[3] TOKYO METROPOLITAN INST MED SCI, DEPT MOL BIOL, BUNKYO KU, TOKYO 113, JAPAN
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 1996年 / 1317卷 / 01期
关键词
Protein kinase C; Isoform; Ischemia; (Rat);
D O I
10.1016/0925-4439(96)00035-X
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
To explore the spatial and temporal localization of PKC isoforms during ischemia, we quantified PKC isoforms in the subcellular fractions in perfused rat heart by immunoblotting using specific antibodies against PKC isoforms. PKCs-alpha and epsilon translocated from the 100 000 X g supernatant (S, cytosolic) fraction to the 1000 x g pellet (P1, nucleus-myofibril) and the 1000-100 000 X g pellet (P2, membrane) fractions during 5-40 min of ischemia. PKC-delta redistributed from the P2 to the S fraction. A 50-kDa fragment of PKC-cu appeared during ischemia possibly through calpain action. Immunohistochemical observations showed the different localizations of PKC-alpha, delta, and epsilon in the myocytes. The PKC assay displayed high basal levels of Ca2+-independent PKC, the activation of Ca2+-dependent PKC in the P1 and P2 fractions, and the activation of Ca2+-independent PKC in the P1 fraction after 20 min of ischemia.
引用
收藏
页码:36 / 44
页数:9
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