INTERLEUKIN-1 AND TUMOR-NECROSIS-FACTOR POTENTIATE ANGIOTENSIN-II-STIMULATED, AND CALCIUM IONOPHORE-STIMULATED PROSTAGLANDIN-E2 SYNTHESIS IN RAT RENAL MESANGIAL CELLS

被引:30
作者
PFEILSCHIFTER, J
MUHL, H
机构
[1] Research Department, Pharmaceuticals Division, Ciba-Geigy Ltd.
关键词
D O I
10.1016/0006-291X(90)90371-S
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
In resting mesangial cells, angiotensin II and the calcium ionophore A23187 stimulated prostaglandin E2 (PGE2) formation. After pretreatment with interleukin 1β (IL-1β) or tumor necrosis factor α (TNFα), which are themselves potent stimuli for PGE2 synthesis, mesangial cells displayed an amplified response to angiotensin II and A23187. The cytokine-induced effects occurred in a time- and dose-dependent manner and were attenuated by actinomycin D, cycloheximide and dexamethasone. IL-1β and TNFα treatment also increased the amount of arachidonic acid released after stimulation of cells with angiotensin II and A23187. In addition, IL-1β but not TNFα treatment augmented the formation of PGE2 from exogenous arachidonic acid by mesangial cells. Furthermore, the conversion of prostaglandin H2 to PGE2 was not changed by IL-1β and TNFα. These results suggest that IL-1β and TNFα exert a priming effect on PGE2 production in mesangial cells. © 1990.
引用
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页码:585 / 595
页数:11
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