Pfeilschifter J, Pignat W, Leighton J, Märki F, Vosbeck K, Alkan S
Research Department, Ciba-Geigy Ltd., Basel, Switzerland.
Biochem J. 1990 Aug 15;270(1):269-71. doi: 10.1042/bj2700269.
Treatment of rat glomerular mesangial cells with transforming growth factor beta 2 (TGF beta 2) stimulates prostaglandin E2 (PGE2) synthesis. Actinomycin D, cycloheximide and diclofenac attenuate the TGF beta 2-induced PGE2 formation. As shown previously, two proinflammatory cytokines, interleukin 1 beta (IL-1 beta) and tumour necrosis factor alpha (TNF alpha), are potent stimuli for PGE2 and phospholipase A2 secretion from mesangial cells. We report here that, whereas TGF beta 2 potentiates the IL-1 beta- and TNF alpha-evoked PGE2 production, it strongly inhibits the phospholipase A2 secretion induced by both cytokines. In addition, the inhibitory effect of TGF beta 2 on phospholipase A2 secretion is not due to the augmented PGE2 formation.
用转化生长因子β2(TGFβ2)处理大鼠肾小球系膜细胞可刺激前列腺素E2(PGE2)的合成。放线菌素D、放线菌酮和双氯芬酸可减弱TGFβ2诱导的PGE2形成。如先前所示,两种促炎细胞因子,白细胞介素1β(IL-1β)和肿瘤坏死因子α(TNFα),是系膜细胞分泌PGE2和磷脂酶A2的有效刺激物。我们在此报告,虽然TGFβ2增强了IL-1β和TNFα诱发的PGE2产生,但它强烈抑制这两种细胞因子诱导的磷脂酶A2分泌。此外,TGFβ2对磷脂酶A2分泌的抑制作用并非由于PGE2形成增加所致。