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SENP1抑制脂多糖诱导的BV2小胶质细胞凋亡和一氧化氮生成。

SENP1 inhibits the IH-induced apoptosis and nitric oxide production in BV2 microglial cells.

作者信息

Liu Song, Wang Zhong-hua, Xu Bo, Chen Kui, Sun Jin-yuan, Ren Lian-ping

机构信息

Department of Respiratory Medicine, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200092, China.

Department of Medical Oncology, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.

出版信息

Biochem Biophys Res Commun. 2015 Nov 27;467(4):651-6. doi: 10.1016/j.bbrc.2015.10.092. Epub 2015 Oct 21.

Abstract

To reveal SUMOylation and the roles of Sentrin-specific proteases (SENP)s in microglial cells under Intermittent hypoxia (IH) condition would provide more intensive view of understanding the mechanisms of IH-induced central nervous system (CNS) damage. Hence, in the present study, we detected the expression levels of SENPs in microglial cells under IH and normoxia conditions via RT-PCR assay. We found that SENP1 was significantly down-regulated in cells exposure to IH. Subsequently, the effect of IH for the activation of microglia and the potential roles of SENP1 in the SENP1-overexpressing cell lines were investigated via Western blotting, RT-PCR and Griess assay. The present study demonstrated the apoptosis-inducing and activating role of IH on microglia. In addition, we revealed that the effect of IH on BV-2 including apoptosis, nitric oxide synthase (iNOS) expression and nitric oxide (NO) induction can be attenuated by SENP1 overexpression. The results of the present study are of both theoretical and therapeutic significance to explore the potential roles of SENP1 under IH condition and elucidated the mechanisms underlying microglial survival and activation.

摘要

揭示小胶质细胞在间歇性缺氧(IH)条件下的类泛素化修饰及类泛素特异性蛋白酶(SENP)的作用,将有助于更深入地理解IH诱导中枢神经系统(CNS)损伤的机制。因此,在本研究中,我们通过逆转录聚合酶链反应(RT-PCR)检测了常氧和IH条件下小胶质细胞中SENP的表达水平。我们发现,暴露于IH的细胞中SENP1显著下调。随后,通过蛋白质免疫印迹法(Western blotting)、RT-PCR和格里斯试剂法(Griess assay)研究了IH对小胶质细胞激活的影响以及SENP1在过表达SENP1细胞系中的潜在作用。本研究证明了IH对小胶质细胞具有诱导凋亡和激活的作用。此外,我们还发现,过表达SENP1可减弱IH对BV-2细胞的影响,包括凋亡、一氧化氮合酶(iNOS)表达和一氧化氮(NO)生成。本研究结果对于探索IH条件下SENP1的潜在作用以及阐明小胶质细胞存活和激活的机制具有理论和治疗意义。

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