KH-type splicing regulatory protein mediate inflammatory response in gastric epithelial cells induced by lipopolysaccharide

被引:12
作者
Chen, Chong [1 ]
Cao, Mei [2 ]
Wu, Daoyan [1 ]
Li, Ningzhe [1 ]
Peng, Jingshan [1 ]
Song, Liju [1 ]
Qi, Panpan [1 ]
Zhang, Mao [2 ]
Zhao, Jian [1 ]
机构
[1] Sichuan Univ, Coll Life Sci, Key Lab Biol Resource & Ecol Environm, Chinese Educ Minist, Chengdu 610064, Sichuan, Peoples R China
[2] Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Core Lab, Chengdu 610072, Sichuan, Peoples R China
基金
中国国家自然科学基金;
关键词
GES-1; cells; immunity; inflammation; KSRP; NF-B signal pathway; NF-KAPPA-B; RAW; 264.7; MACROPHAGES; MESSENGER-RNA DECAY; RAW264.7; SIGNALING PATHWAYS; NITRIC-OXIDE; ACTIVATION; KSRP; INHIBITION;
D O I
10.1002/cbin.10804
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
To study differential expressions of KH-type splicing regulatory protein (KSRP) and inflammatory factors and to explore the relationship between them in Lipopolysaccharide (LPS)-induced gastric epithelial cells (GES-1), cells were exposed to LPS for 24h in the presence or absence of SC-514. Western blot and real-time PCR (RT-PCR) were used to analysis the contents of KSRP, inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2). The results showed that LPS decreased the expression of KSRP protein in GES-1 cells, but not KSRP mRNA, while increasing the levels of iNOS and COX-2 proteins and mRNAs in GES-1cells. High expression of KSRP induced low expressions and stabilities of iNOS and COX-2 in GES-1 cells, indicated that KSRP protein presented negative correlation with iNOS and COX-2 with LPS stimulation. In conclusion, the regulation of expression of KSRP was mainly achieved through post-translational modification. KSRP protein participated in regulating the expression of iNOS and COX-2 in their transcription and translation levels. In response to LPS or gram negative pathogenic microorganism, KSRP could regulate Toll-like receptor (TLR)/ Nuclear factor-kappa B (NF-B) signal pathway in GES-1 cells.
引用
收藏
页码:871 / 878
页数:8
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