hepatocyte growth factor increases vascular endothelial growth factor-a production in human synovial fibroblasts through c-met receptor pathway肝细胞生长因子增加血管内皮生长因子a生产在人体滑膜成纤维细胞通过c-met受体途径.pdfVIP

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hepatocyte growth factor increases vascular endothelial growth factor-a production in human synovial fibroblasts through c-met receptor pathway肝细胞生长因子增加血管内皮生长因子a生产在人体滑膜成纤维细胞通过c-met受体途径.pdf

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hepatocyte growth factor increases vascular endothelial growth factor-a production in human synovial fibroblasts through c-met receptor pathway肝细胞生长因子增加血管内皮生长因子a生产在人体滑膜成纤维细胞通过c-met受体途径

Hepatocyte Growth Factor Increases Vascular Endothelial Growth Factor-A Production in Human Synovial Fibroblasts through c-Met Receptor Pathway 1,2 3 4,5 4,6 1 7,8 Yu-Min Lin , Yuan-Li Huang , Yi-Chin Fong , Chun-Hao Tsai , Ming-Chih Chou , Chih-Hsin Tang * 1 Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan, 2 Department of Orthopedic Surgery, Taichung Veterans General Hospital, Taichung, Taiwan, 3 Department of Biotechnology, College of Health Science, Asia University, Taichung, Taiwan, 4 Department of Orthopaedic Surgery, China Medical University Hospital, Taichung, Taiwan, 5 School of Chinese Medicine, China Medical University, Taichung, Taiwan, 6 Department of Medicine and Graduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan, 7 Department of Pharmacology, School of Medicine, China Medical University, Taichung, Taiwan, 8 Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan Abstract Background: Angiogenesis is essential for the progression of osteoarthritis (OA). Hepatocyte growth factor (HGF) is an angiogenic mediator, and it shows elevated levels in regions of OA. However, the relationship between HGF and vascular endothelial growth factor (VEGF-A) in OA synovial fibroblasts (OASFs) is mostly unknown. Methodology/Principal Findings: Here we found that stimulation of OASFs with HGF induced concentration- and time- dependent increases in VEGF-A expression. Pretreatment with PI3K inhibitor (Ly294002), Akt inhibitor, or mTORC1 inhibitor (rapamycin) blocked the HGF-induced VEGF-A production. Treatment of cells with HGF also increased PI3K, Akt, and mTORC1 phosphorylation. Furt