敲低 SENP7 抑制了 Raw 264.7 细胞中的细胞焦亡和 NF-κB/NLRP3 炎性体途径的激活。
SENP7 knockdown inhibited pyroptosis and NF-κB/NLRP3 inflammasome pathway activation in Raw 264.7 cells.
机构信息
Department of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Department of Obstetrics and Gynaecology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
出版信息
Sci Rep. 2020 Oct 1;10(1):16265. doi: 10.1038/s41598-020-73400-w.
Pyroptosis is a kind of necrotic and inflammatory programmed cell death induced by inflammatory caspases. SENP7 is a SUMO-specific protease, which mainly acts on deconjugation of SUMOs from substrate proteins. We evaluated the effect of SENP7 knockdown on pyroptosis, NF-κB signaling pathway, and NLRP3 inflammasome in Raw 264.7 cells. The results showed that the GSDMD protein mainly expressed in the cytoplasm nearby nuclei of Raw 264.7 cells. It migrated to cytomembrane with the numbers of Raw 264.7 cell decreased when LPS + ATP were administrated. Which was inhibited by SENP7 knockdown. In addition, not only the pyroptosis of Raw 264.7 cells was inhibited, the activation of NF-κB signaling pathway and NLRP3 inflammasome were also attenuated by SENP7 knockdown. The mechanism may be associated with the over SUMOylation of proteins induced by SENP7 knockdown.
细胞焦亡是一种由炎性半胱天冬酶诱导的、依赖于炎性小体的细胞程序性坏死。SENP7 是一种 SUMO 特异性蛋白酶，主要作用是将 SUMO 从底物蛋白上切割下来。我们评估了 SENP7 敲低对 Raw 264.7 细胞中细胞焦亡、NF-κB 信号通路和 NLRP3 炎性小体的影响。结果表明，GSDMD 蛋白主要在 Raw 264.7 细胞的细胞质中靠近核的位置表达。当 LPS+ATP 给药时，GSDMD 蛋白从细胞质向细胞膜转位，Raw 264.7 细胞数量减少，这种转位被 SENP7 敲低所抑制。此外，SENP7 敲低不仅抑制了 Raw 264.7 细胞的焦亡，还抑制了 NF-κB 信号通路和 NLRP3 炎性小体的激活。其机制可能与 SENP7 敲低诱导的蛋白质 SUMO 化过度有关。
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