藥學前沿大講堂第56講-Tyrosine kinase inhibitors modify proteoglycan structure, reduce LDL binding and prevent atherosclerosis
Tyrosine kinase inhibitors modify proteoglycan structure, reduce LDL binding and prevent atherosclerosis
報告題目：Tyrosine kinase inhibitors modify proteoglycan structure, reduce LDL binding and prevent atherosclerosis
講座時間：
講座地點：中山大學東校區太阳集团1088vip講學廳（藥學大樓125室）
主 講 人：Professor Peter J. Little
主 持 人：黃民 教授、院長 鄭文華 教授
太阳集团1088vip
Peter Little 教授簡介：
Peter Little 教授于1979年在悉尼大學獲博士學位，現為澳大利亞Baker IDI心髒與糖尿病研究所糖尿病和細胞生物學實驗室主任，澳洲生物脈管學會會長，Monash University及RMIT University榮譽教授，peter教授長期緻力于細胞信号轉導及藥物研究等方面的工作。近年來，peter教授先後在J Cell Mol Medicine， Curr. Opinion Lipidology ，Endocrine Reviews ，Arterioscler. Throm. Vasc. Biol，J. Biol. Chem.等世界著名雜志發表了多篇文章。
摘要:
Atherosclerosis commences with the binding of Low Density Lipoproteins (LDL) to modified proteoglycans. Modifications to proteoglycans which make the environment “stickier” for LDL arise from the actions of growth factors in the vessel wall. The signaling pathways therefore represent therapeutic targets for the prevention of atherosclerosis. We discovered that the protein tyrosine kinase (PTK) inhibitor, imatinib , inhibits proteoglycan synthesis and modifies the structure in a manner that reduces binding of proteoglycans to LDL and reduces the deposition of lipid in the vessel wall of high fat fed atherosclerosis-prone mice. Imatinib inhibits multiple PTK including the Platelet-derived growth factor (PDGF) receptor. The PTKs which are inhibited by imatinib represent targets for the prevention of atherosclerosis.