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        Nitro-oleic Acid Decreases Transcription of the Angiotensin II Type I Receptor Gene in Aortic Smooth Muscle Cells

        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.

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        Omp16, a conserved peptidoglycan-associated lipoprotein, is involved in Brucella virulence in vitro

        Feijie Zhi,Dong Zhou,Junmei Li,Lulu Tian,Guangdong Zhang,Yaping Jin,Aihua Wang 한국미생물학회 2020 The journal of microbiology Vol.58 No.9

        Brucella, the bacterial agent of common zoonotic brucellosis, primarily infects specific animal species. The Brucella outer membrane proteins (Omps) are particularly attractive for developing vaccine and improving diagnostic tests and are associated with the virulence of smooth Brucella strains. Omp16 is a homologue to peptidoglycan-associated lipoproteins (Pals), and an omp16 mutant has not been generated in any Brucella strain until now. Very little is known about the functions and pathogenic mechanisms of Omp16 in Brucella. Here, we confirmed that Omp16 has a conserved Pal domain and is highly conserved in Brucella. We attempted to delete omp16 in Brucella suis vaccine strain 2 (B. suis S2) without success, which shows that Omp16 is vital for Brucella survival. We acquired a B. suis S2 Omp16 mutant via conditional complementation. Omp16 deficiency impaired Brucella outer membrane integrity and activity in vitro. Moreover, inactivation of Omp16 decreased bacterial intracellular survival in macrophage RAW 264.7 cells. B. suis S2 and its derivatives induced marked expression of IL-1β, IL-6, and TNF-α mRNA in Raw 264.7 cells. Whereas inactivation of Omp16 in Brucella enhanced IL-1β and IL-6 expression in Raw 264.7 cells. Altogether, these findings show that the Brucella Omp16 mutant was obtained via conditional complementation and confirmed that Omp16 can maintain outer membrane integrity and be involved in bacterial virulence in Brucella in vitro and in vivo. These results will be important in uncovering the pathogenic mechanisms of Brucella.

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