Simmons D L, Xie W, Evett G, Merrill J, Robertson D L, Bradshaw W S
Department of Chemistry, Brigham Young University, Provo, UT 84602.
J Lipid Mediat. 1993 Mar-Apr;6(1-3):113-7.
Prostaglandin G/H synthase isoenzyme 2 (PGHS-2) was identified as an immediate-early gene product induced by Rous sarcoma virus, serum, phorbol ester and a wide variety of other mitogens. Induction of PGHS-2 occurs through an increase in PGHS-2 gene transcription. Dexamethasone inhibits both the basal and induced levels of PGHS-2 mRNA. In contrast, PGHS-1 gene transcription rate, mRNA, and protein levels are unaffected by mitogens and dexamethasone. Post-transcriptional down-regulation of PGHS-2 mRNA plays a significant role in causing dexamethasone's effect. Specific cell systems have been identified which allow selective analysis of PGHS-1 and PGHS-2 at the nucleic acid and protein levels. These cell systems indicate that PGHS-1 and PGHS-2 may have different sensitivities to non-steroidal anti-inflammatory drugs. Furthermore, inhibition of PGHS activity correlates well with suppression of the transformed phenotype in an in vitro cell model.
前列腺素G/H合成酶同工酶2（PGHS-2）被鉴定为一种由劳氏肉瘤病毒、血清、佛波酯和多种其他有丝分裂原诱导产生的即刻早期基因产物。PGHS-2的诱导是通过PGHS-2基因转录增加实现的。地塞米松可抑制PGHS-2 mRNA的基础水平和诱导水平。相比之下，PGHS-1基因的转录速率、mRNA和蛋白质水平不受有丝分裂原和地塞米松的影响。PGHS-2 mRNA的转录后下调在导致地塞米松的作用方面起着重要作用。已经确定了特定的细胞系统，可在核酸和蛋白质水平上对PGHS-1和PGHS-2进行选择性分析。这些细胞系统表明，PGHS-1和PGHS-2对非甾体抗炎药可能具有不同的敏感性。此外，在体外细胞模型中，PGHS活性的抑制与转化表型的抑制密切相关。
