CCN1 Induces Oncostatin M Production in Osteoblasts via Integrin-Dependent Signal Pathways

ASIA unversity > 醫學暨健康學院 > 生物科技學系 > 期刊論文 > Item 310904400/81248

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题名:	CCN1 Induces Oncostatin M Production in Osteoblasts via Integrin-Dependent Signal Pathways
作者:	Cheng-Yu Che(Cheng-Yu Chen)、Chen-Ming Su(Chen-Ming Su)、黃元勵(HUANG, YUAN-LI)、Chun-Hao Tsa(Chun-Hao Tsai)、Lih-Jyh Fuh(Lih-Jyh Fuh)、湯智昕(Chih-Hsin, Tang)*
贡献者:	生物科技學系
日期:	201409
上传时间:	2014-10-08 05:54:13 (UTC+0)
摘要:	Inflammatory response and articular destruction are common symptoms of osteoarthritis. Cysteine-rich 61 (CCN1 or Cyr61), a secreted protein from the CCN family, is associated with the extracellular matrix involved in many cellular activities like growth and differentiation. Yet the mechanism of CCN1 interacting with arthritic inflammatory response is unclear. This study finds CCN1 increasing expression of oncostatin m (OSM) in human osteoblastic cells. Pretreatment of αvβ3 monoclonal antibody and inhibitors of focal adhesion kinase (FAK), c-Src, phosphatidylinositol 3-kinase (PI3K), and NF-κB inhibited CCN1-induced OSM expression in osteoblastic cells. Stimulation of cells with CCN1 increased phosphorylation of FAK, c-Src, PI3K, and NF-κB via αvβ3 receptor; CCN1 treatment of osteoblasts increased NF-κB-luciferase activity and p65 binding to NF-κB element on OSM promoter. Results indicate CCN1 heightening OSM expression via αvβ3 receptor, FAK, c-Src, PI3K, and NF-κB signal pathway in osteoblastic cells, suggesting CCN1 as a novel target in arthritis treatment.
關聯:	PLoS One
显示于类别:	[生物科技學系] 期刊論文

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