ANPs effect on MARCKS and StAR phosphorylation in agonist-stimulated glomerulosa cells

被引:12
作者
Calle, RA
Bollag, WB
White, S
Betancourt-Calle, S
Kent, P
机构
[1] Med Coll Georgia, Inst Mol Med & Genet, Program Cell Signaling, Augusta, GA 30912 USA
[2] Med Coll Georgia, Dept Cellular Biol & Anat, Augusta, GA 30912 USA
[3] Augusta Vet Affairs Med Ctr, Dept Endocrinol, Augusta, GA USA
关键词
aldosterone; adrenal glomerulosa; angiotensin II; potassium; myristoylated alanine-rich C-kinase substrate; steroidogenic acute regulatory protein;
D O I
10.1016/S0303-7207(01)00454-3
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Atrial natriuretic peptide (ANP) is a cardiac hormone that inhibits aldosterone secretion induced by all physiologic agonists. The purpose of this study is to explore ANP-induced changes in the phosphorylation of myristoylated alanine-rich C-kinase substrate (MARCKS) and the steroidogenic acute regulatory protein (StAR), in AngII or K+-stimulated glomerulosa cells. The data show that ANP completely inhibits the phosphorylation of MARCKS and partially inhibits that of StAR in cells stimulated with K+. ANP also partially inhibits MARCKS phosphorylation but does not affect StAR phosphorylation in cells stimulated with AngII. These effects appear to be cGMP-independent and at least partially dependent on inhibition of protein kinase C (PKC). To our knowledge, this is the first report of ANP modulating either MARCKS or StAR phosphorylation in [P-32]-labeled cells. The data also support the hypothesis that ANP inhibits aldosterone secretion acting as a step involved in cholesterol transport to the mitochondria. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:71 / 79
页数:9
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