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Okadaic acid interferes with lipoprotein-supported corticosterone production in adrenal cells.

Abstract：

:Rat adrenocortical cells in culture respond to stimulation by ACTH alone (15 fold over basal) and to ACTH + added lipoproteins (as an exogeneous source of cholesterol), with an additional 25-30 fold rise in steroidogenesis. With the addition of okadaic acid (OKA, 100 nM), a potent protein phosphatase inhibitor, the lipoprotein-induced rise in steroidogenesis is blocked. If 20 alpha-hydroxycholesterol is provided instead of lipoprotein-cholesterol, OKA has no effect suggesting that OKA affects only actively transported cholesterol. Since the OKA block is preceded by specific morphological changes in the cell (i.e., the loss of Golgi-associated microtubules followed by the disruption of the Golgi apparatus itself), it is hypothesized that some OKA-sensitive phosphoprotein associated with the microtubule/Golgi network of adrenocortical cells is critical for lipoprotein-derived cholesterol uptake and/or transport during steroidogenesis.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Azhar S,Wang H,Tsai L,Reaven E

doi

10.1016/0006-291x(91)91877-f

subject

Has Abstract

pub_date

1991-09-16 00:00:00

pages

726-33

issue

2

eissn

0006-291X

issn

1090-2104

pii

0006-291X(91)91877-F

journal_volume

179

pub_type

杂志文章

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