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首页> 外文期刊>American Journal of Physiology >Nitric oxide stimulates COX-2 expression in cultured collecting duct cells through MAP kinases and superoxide but not cGMP.
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Nitric oxide stimulates COX-2 expression in cultured collecting duct cells through MAP kinases and superoxide but not cGMP.

机译：一氧化氮通过MAP激酶和超氧化物刺激cXMP刺激COX-2在培养的集合管细胞中的表达。

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摘要

Collecting ducts are a major site of renal production and action of both prostaglandins and nitric oxide. Experiments were undertaken to examine whether nitric oxide regulates cyclooxygenase (COX)-2 expression and PGE(2) release in cultured collecting duct cells. In mIMCD-K2 cells, sodium nitroprusside (SNP) in the 50- to 800-microM range induced a marked dose- and time-dependent increase in COX-2 protein levels, determined by immunoblotting, and the induction was detectable at 4 h. This was preceded by induction of COX-2 mRNA as determined by real-time-RT-PCR. The COX-2 induction was accompanied by a significant rise in PGE(2) release as determined by enzyme immunoassay. S-nitroso-N-acetylpenicillamine (SNAP) had a similar stimulatory effect on COX-2 expression and PGE(2) release. 8-bromo-cGMP (200 microM) had no effect on COX-2 expression. The SNP-stimulated COX-2 expression was not affected by the guanylyl cyclase inhibitor methylene blue or the protein kinase G inhibitor KT-5823 (2.0 microM). In contrast, the SNP-stimulated COX-2 expression was significantly reduced by either the Erk1/2 inhibitor PD-98059 or the P38 inhibitor SB-203580 and was abolished by combination of the two kinase inhibitors. The stimulation was also significantly blocked by the SOD mimetic tempol. Thus we conclude that NO stimulates COX-2 expression in collecting duct cells through mechanisms involving MAP kinase and superoxide, but not cGMP.
机译：收集导管是肾脏产生以及前列腺素和一氧化氮的主要作用部位。进行实验以检查一氧化氮是否调节培养的收集导管细胞中的环氧合酶（COX）-2表达和PGE（2）释放。在mIMCD-K2细胞中，硝普钠（SNP）在50至800 microM范围内，可通过免疫印迹法检测到明显的剂量和时间依赖性的COX-2蛋白水平增加，且在4 h时可检测到这种诱导作用。在此之前通过实时RT-PCR确定诱导COX-2 mRNA。通过酶免疫法测定，COX-2诱导伴随着PGE（2）释放的显着增加。 S-亚硝基-N-乙酰青霉胺（SNAP）对COX-2表达和PGE（2）释放具有类似的刺激作用。 8-溴-cGMP（200 microM）对COX-2表达没有影响。 SNP刺激的COX-2表达不受鸟苷基环化酶抑制剂亚甲基蓝或蛋白激酶G抑制剂KT-5823（2.0 microM）的影响。相反，Erk1 / 2抑制剂PD-98059或P38抑制剂SB-203580显着降低了SNP刺激的COX-2表达，而两种激酶抑制剂的组合则废除了SNP刺激的COX-2表达。刺激也被SOD模拟的tempol显着阻断。因此，我们得出结论，NO可以通过涉及MAP激酶和超氧化物但不刺激cGMP的机制刺激集合管细胞中COX-2的表达。

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