CircFndc3b通过调控巨噬细胞分化抑制病理性心肌肥厚  

CircFndc3b alleviates pathological cardiac hypertrophy by regulating macrophage differentiation

作　　者：孙仕泽 赵之 孙伟[3] SUN Shize;ZHAO Zhi;SUN Wei(Department of Coronary Heart Disease,Dalian Central Hospital,Dalian 116089,China;Department of Ultrason-graphy,Affiliated Zhongshan Hospital of Dalian University,Dalian 116000,China;Department of Cardiology,Da-lian Third People's Hospital,Dalian 116091,China)

机构地区：[1]大连市中心医院冠心病一科,116089 [2]大连大学附属中山医院超声科,116000 [3]大连市第三人民医院心内科,116091

出　　处：《免疫学杂志》2022年第9期796-803,共8页Immunological Journal

摘　　要：目的探讨CircFndc3b调控巨噬细胞分化抑制病理性心肌肥厚及相关机制。方法临床征集40例心衰患者血清样本,选择10只自然衰老导致的心衰小鼠。荧光定量PCR检测患者血清和小鼠心脏组织中CircFndc3b表达。年轻和心衰小鼠分别尾静脉注射抑制CircFndc3b和过表达CircFndc3b的腺相关病毒,检测小鼠心功能和病理性肥厚相关变化以及M1/M2巨噬细胞比例变化。结果荧光定量PCR结果显示,心衰患者血清中CircFndc3b表达升高(P<0.05),心衰小鼠心脏组织中CircF⁃ndc3b表达升高(P<0.05)。与年轻小鼠比较,心衰小鼠心功能变弱,M1/M2型巨噬细胞比例降低,心肌细胞明显变大,ANP和BNP表达明显升高,纤维化水平升高(P<0.05)。心衰小鼠尾静脉注射AAV-OE-CircFndc3b后,小鼠心功能变强,M1/M2型巨噬细胞比例升高,心肌细胞明显变小,ANP和BNP表达降低,纤维化水平降低(P<0.05)。心衰小鼠尾静脉注射AAV-sh-CircFndc3b后,小鼠心功能更加恶化,M1/M2型巨噬细胞比例进一步降低,心肌细胞变为最小,ANP和BNP表达明显升高,纤维化水平进一步升高(P<0.05)。结论过表达CircFndc3b通过调控脾脏巨噬细胞分化抑制病理性心肌肥厚。To explore the mechanisms of CircFndc3b in regulating macrophage differentiation and alleviating pathological cardiac hypertrophy.Serum samples from 40 patients with heart failure and 10 mice with heart failure caused by natural aging were collected for detection of CircFndc3b expression in serum and tissues by fluorescence quantitative PCR.Young and old mice were injected with AAV-OE-CircFndc3b and AAV-sh-CircFndc3b by tail vein,respectively,and the changes of heart function,pathological hypertrophy and the proportion of M1/M2 macrophages were detected.Fluorescence quantitative PCR results showed that CircFndc3b expression was increased in the serum of patients with heart failure(P<0.05),and in heart tissue of mice(P<0.05).Compared with young mice,the heart function of old mice was weakened,the proportion of M1/M2 macrophages was decreased,the myocardial cells were significantly enlarged,the expression of ANP and BNP were significantly increased,and the level of fibrosis was increased(P<0.05).After AAV-OE-CircFndc3b was injected into the tail vein of old mice,the heart function of the mice became stronger,the proportion of M1/M2 macrophages increased,the myocardial cells became significantly smaller,the expression of ANP and BNP decreased,and the fibrosis level decreased(P<0.05).After AAV-sh-CircFndc3b was injected into the tail vein of old mice,the cardiac function of the mice became worse,the proportion of M1/M2 macrophages was further reduced,the myocardial cells became the minimum,the expression of ANP and BNP was significantly increased,and the fibrosis level was further increased(P<0.05).In conclusion,CircFndc3b alleviates pathological cardiac hypertrophy by regulating macrophage differentiation.

关 键 词：CircFndc3b M1/M2巨噬细胞分化 心衰诊断 

分 类 号：R714.252[医药卫生—妇产科学]