Requirement of the phosphatidylinositol 3-kinase/Akt signaling pathway for the effect of nicotine on interleukin-1beta-induced chondrocyte apoptosis in a rat model of osteoarthritis

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	Requirement of the phosphatidylinositol 3-kinase/Akt signaling pathway for the effect of nicotine on interleukin-1beta-induced chondrocyte apoptosis in a rat model of osteoarthritis
	Zheng, Xinpeng ; Xia, Chun ; Chen, Zhongyi ; Huang, Jiagu ; Gao, Fengguang ; Li, Guideng ; Zhang, Bing ; Xia C(夏春) ; Gao FG(高丰光) ; Zhang B(张兵)
刊名	http://dx.doi.org/10.1016/j.bbrc.2012.06.045
	2012-07-06
关键词	MATRIX METALLOPROTEINASE-13 EXPRESSION ARTICULAR CHONDROCYTES PROTEIN-KINASE PROTEOGLYCAN SYNTHESIS CELL-DEATH CARTILAGE ACTIVATION GROWTH PHOSPHORYLATION INHIBITOR
英文摘要	National Natural Science Foundation of China [81072015]; Natural Science Foundation of Fujian, China [2010D007]; Medical Innovation Foundation of Fujian, China [2011-CXB-36]; Xiamen Science and Technology Key program grant, Fujian, China; Chondrocyte apoptosis is mainly responsible for the progressive degeneration of cartilage in osteoarthritis (OA). Interleukin-1beta (IL-1 beta) was widely used as a modulating and chondrocyte apoptosis-inducing agent. Nicotine is able to confer resistance to apoptosis and promote cell survival in some cell lines, but its regulatory mechanism is ambiguous. We aimed to investigate the effect of nicotine on IL-1 beta-induced chondrocyte apoptosis and the mechanism underlying how nicotine antagonizes IL-1 beta-induced apoptosis of rat chondrocytes. Chondrocytes isolated from newborn rat joints were exposed to IL-1 beta. The cell viability was analyzed by the MTT (3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl tetrazolium bromide) assay, and the apoptotic cells were counted with DAPI staining. The levels of Akt, phosphorylated-Akt (p-Akt) and downstream protein targets of Akt were detected by western blotting. The results showed that nicotine neutralized the effect of IL-1 beta on chondrocytes by activating PI3K/Akt signaling pathways, including the PI3K/Akt/Bcl-2 pathway, to block IL-1 beta-induced cell apoptosis and the PI3K/Akt/p70S6K (p70S6 kinase)/S6 pathway for promoting protein synthesis, modulating its downstream effectors such as TIMP-1 and MMP-13. Activation of the PI3K/Akt pathway is, in part, required for the effect of nicotine on IL-1 beta-induced chondrocyte apoptosis in a rat model of osteoarthritis. (C) 2012 Elsevier Inc. All rights reserved.
语种	英语
出版者	BIOCHEM BIOPH RES CO
内容类型	期刊论文
源URL	[http://dspace.xmu.edu.cn/handle/2288/93350]
专题	医学院－已发表论文
推荐引用方式 GB/T 7714	Zheng, Xinpeng,Xia, Chun,Chen, Zhongyi,et al. Requirement of the phosphatidylinositol 3-kinase/Akt signaling pathway for the effect of nicotine on interleukin-1beta-induced chondrocyte apoptosis in a rat model of osteoarthritis[J]. http://dx.doi.org/10.1016/j.bbrc.2012.06.045,2012.
APA	Zheng, Xinpeng.,Xia, Chun.,Chen, Zhongyi.,Huang, Jiagu.,Gao, Fengguang.,...&张兵.(2012).Requirement of the phosphatidylinositol 3-kinase/Akt signaling pathway for the effect of nicotine on interleukin-1beta-induced chondrocyte apoptosis in a rat model of osteoarthritis.http://dx.doi.org/10.1016/j.bbrc.2012.06.045.
MLA	Zheng, Xinpeng,et al."Requirement of the phosphatidylinositol 3-kinase/Akt signaling pathway for the effect of nicotine on interleukin-1beta-induced chondrocyte apoptosis in a rat model of osteoarthritis".http://dx.doi.org/10.1016/j.bbrc.2012.06.045 (2012).