Macrophage-Stimulated Cardiac Fibroblast Production of IL-6 Is Essential for TGF β/Smad Activation a

• 作 者: FeifeiMa[1]YulinLi[2]LixinJia;YaleiHan;JizhongCheng;HuihuaLi;YongfenQi;JieDu;
• 机 构: Beijing An Zhen Hospital, Capital Medical University, Beijing, China
• 出 处: 第七届北京五洲心血管病研讨会
• 发表日期: 2013年期

　　Interleukin6 (IL6) is an important cytokine participating in multiple biologic activities in immune regulation and inflammation.IL6 has been associated with cardiovascular remodeling.However,the mechanism of IL6 in hypertensive cardiac fibrosis is still unclear.Angiotensin Ⅱ (Ang Ⅱ) infusion in mice increased IL6 expression in the heart.IL6 knockout (IL6/) reduced Ang Ⅱinduced cardiac fibrosis:1) Masson trichrome staining showed that Ang I1 infusion significantly increased fibrotic areas of the wild,pe mouse heart,which was greatly suppressed in IL6/ mice and 2) immunohistochemistry staining showed decreased expression of asmooth muscle actin (aSMA),transforming growth factor β 1 (TGF β 1) and collagen I in IL6/ mouse heart.The baseline mRNA expression of 1L6 in cardiac fibroblasts was low and was absent in cardiomyocytes or macrophages; however,co culture of cardiac fibroblasts with maerophages significantly increased IL6 production and expression of aSMA and collagen I in fibroblasts.