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作 者:WANG Yu Peng WANG Ping DONG Lei CHEN Hui WU Yong Quan LI Hong Wei LI Min
机构地区:[1]Health and Heart Center, the Beijing Friendship Hospital affiliated the Capital Medical University [2]Cardiovascular Center, the Beijing Friendship Hospital affiliated the Capital Medical University
出 处:《Biomedical and Environmental Sciences》2014年第2期138-141,共4页生物医学与环境科学(英文版)
基 金:This work was supported by the National Natural Science Foundation of China(Grant NoS.81100169).
摘 要:Relaxin is known to inhibit cardiac fibrosis. However, it is unclear whether relaxin could regulate the effects of Phorbol 12-myristate 13-acetate (PMA, PKC activator) on cardiac fibrosis. So the influence of relaxin on the cell proliferation and collagen expression induced by PMA in cultured cardiac fibroblasts was studied. It showed that PMA significantly increased cardiac fibroblasts proliferation, Type I pro-collagen protein expression, Type I pro-collagen mRNA expression, and rhRLX absolutely significantly decreased PMA induced effects on cardiac fibroblasts proliferation and Type I pro-collagen expressions, indicating that relaxin could inhibit cardiac fibrosis induced by PMA.Relaxin is known to inhibit cardiac fibrosis. However, it is unclear whether relaxin could regulate the effects of Phorbol 12-myristate 13-acetate (PMA, PKC activator) on cardiac fibrosis. So the influence of relaxin on the cell proliferation and collagen expression induced by PMA in cultured cardiac fibroblasts was studied. It showed that PMA significantly increased cardiac fibroblasts proliferation, Type I pro-collagen protein expression, Type I pro-collagen mRNA expression, and rhRLX absolutely significantly decreased PMA induced effects on cardiac fibroblasts proliferation and Type I pro-collagen expressions, indicating that relaxin could inhibit cardiac fibrosis induced by PMA.
关 键 词:PKC Figure PMA Relaxin Inhibit Cardiac Fibrosis Induced by Phorbol 12-myristate 13-acetate
分 类 号:R542[医药卫生—心血管疾病]
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