VARIATIONS IN GUANINE-BINDING PROTEINS (GS, GI) IN CULTURED BOVINE ADRENAL-CELLS - CONSEQUENCES ON THE EFFECTS OF PHORBOL ESTER AND ANGIOTENSIN-II ON ADRENOCORTICOTROPIN-INDUCED AND CHOLERA-TOXIN-INDUCED CAMP PRODUCTION
VARIATIONS IN GUANINE-BINDING PROTEINS (GS, GI) IN CULTURED BOVINE ADRENAL-CELLS - CONSEQUENCES ON THE EFFECTS OF PHORBOL ESTER AND ANGIOTENSIN-II ON ADRENOCORTICOTROPIN-INDUCED AND CHOLERA-TOXIN-INDUCED CAMP PRODUCTION
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DOI：
10.1111/j.1432-1033.1988.tb14100.x
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发表时间：
1988-06-01
期刊：
影响因子：
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通讯作者：
SAEZ, JM
中科院分区：
文献类型：
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作者：
BEGEOT, M;LANGLOIS, D;SAEZ, JM
培养的牛肾上腺细胞经促肾上腺皮质激素(ACTH)或霍乱毒素诱导的cAMP产量在培养第0~7天呈递增趋势。血管紧张素II(A-II)抑制基础和ACTH刺激的肾上腺原膜腺苷环化酶，对ACTH或霍乱毒素诱导的新鲜分离细胞(第0天)产生cAMP无影响，但从第0d起逐渐增强这两种效应物的刺激作用。培养1~7天。相反，佛波酯对新鲜分离的细胞有增强作用。细胞经百日咳毒素处理后，在培养0~3d，A-II对细胞的增强作用增强，但在培养7d后增强作用不明显。用霍乱毒素(核糖化αs蛋白)或百日咳毒素(αi蛋白)对新鲜分离或培养的肾上腺细胞膜进行ADP核糖基化后，αs增加，αi显著降低，培养第0、3和7天的αi/αs分别为4、0.6和0.1。这些结果表明：(A)A-II对ACTH或霍乱毒素诱导的cAMP的产生具有双重作用：一种是由GI介导的抑制，另一种是由蛋白激酶C激活介导的刺激作用，这可以解释A-II对新鲜细胞没有明显作用的原因；(B)A-II的增强作用可能是由于αi的逐渐减少，而αs的逐渐增加可以解释培养细胞对ACTH或霍乱毒素的反应性增强。
The corticotropin (ACTH) or cholera-toxin-induced cAMP production by cultured bovine adrenal cells increased progressively between days 0 and 7 of culture. Angiotensin II (A-II), which inhibited both basal and ACTH-stimulated adenylate cyclase of crude adrenal membranes, had no effect on ACTH-induced or cholera-toxin-induced cAMP production by fresh isolated cells (day 0) but progressively potentiated the stimulatory action of both effectors from day 0 .fwdarw. 1 to day 7 of culture. In contrast, phorbol ester had a potentiating effect on fresh isolated cells. Pretreatment of cells with pertussis toxin enhanced the potentiating effect of A-II on cells between 0 and 3 days of culture, but not after 7 days. ADP-ribosylation by cholera toxin (ribosylating .alpha.s proteins) or pertussis toxin (.alpha.i proteins), of adrenal membranes prepared from fresh isolated or cultured cells revealed an increase in .alpha.s and a dramatic decrease in .alpha.i, the ratios .alpha.i/.alpha.s on day 0, 3 and 7 of culture were 4, 0.6 and 0.1 respectively. These results indicate that (a) A-II had a double effect on ACTH-induced or cholera-toxin-induced cAMP production: one inhibitory mediated by Gi, the other stimulatory mediated by protein kinase C activation; this could explain the lack of apparent effect of A-II on fresh cells; (b) the progressive decrease of .alpha.i might be responsible for the appearance of the potentiating effect of A-II whereas the progressive increase of .alpha.s could explain the enhanced responsiveness to ACTH or cholera toxin of cultured cells.