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Huan Wang,Hongsheng Ouyang,Yaping Tian,Zhuang Liu,Xiaolei Han,Xingxing Liu,Guangyao Ran,Gangqi Wang,Daxin Pang,Xiaochun Tang 한국생물공학회 2014 Biotechnology and Bioprocess Engineering Vol.19 No.4
Nitroalkene derivatives of nitro-oleic acid(OA-NO2) regulate pluripotent cell signaling in vivo underphysiological and pathological conditions. Angiotensin IItype 1 receptor (AT1R) plays an important role in thecardiovascular system. In this study, OA-NO2 reduced theAT1R mRNA level, specifically in primary smooth musclecells, showing a 70% reduction in rat smooth muscle cells(RASMCs) and a 50% reduction in pig smooth musclecells (PASMCs). These effects were not observed in CHOcells, which highly express AT1R. The AT1R mRNA decayrate was unchanged after OA-NO2 compared with OAtreatment. Nitric oxide (NO) and peroxisome proliferatoractivatedreceptor gamma (PPARγ) did not alter thereduced effects of OA-NO2 on the AT1R mRNA level inSMCs. However, Sp1-mediated activation of the AT1Rpromoter was reduced in response to OA-NO2 in RASMCsbut not 293T cells. In addition, the nuclear factor-kappa B(NF-κB) pathway was involved in the OA-NO2-mediateddownregulation of AT1R transcription in SMCs. Takentogether, our results demonstrate that OA-NO2 specificallyinhibits AT1R mRNA expression in primary smooth musclecells via the NF-κB pathway.