C1q/TNF 相关蛋白-2 改善血管生成，在缺血再灌注期间保护心肌功能。
C1q/TNF-related protein-2 improved angiogenesis to protect myocardial function during ischaemia‒reperfusion.
机构信息
Department of Cardiology, 117890Fujian Medical University Union Hospital, Fujian Medical Center for Cardiovascular Diseases, Fujian Institute of Coronary Heart Disease, Fujian Key Laboratory of Vascular Aging, Fujian Medical University, Fujian, China.
Department of Cardiovascular Medicine, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, 66281Shanghai Jiao Tong University School of Medicine, Shanghai, China.
出版信息
Diab Vasc Dis Res. 2022 Nov-Dec;19(6):14791641221137355. doi: 10.1177/14791641221137355.
BACKGROUND
Collateral growth plays an important role in the recovery of acute myocardial infarction. C1q/TNF-related protein-2 (CTRP2), a CTRP family member, showed some protective effects on cell survival. In this study, the relationship between CTRP2 and collateral growth was examined.
METHODS
C57BL/6 mice were subjected to myocardial ischaemia/reperfusion (I/R), and the expression of CTRP2 and the effect of CTRP2 on infarction size, cardiac function and angiogenesis were examined. The ischaemic hindlimb model was also used to examine the effect of CTRP2. In vitro, CTRP2-mediated regulation of angiogenesis, AKT activation and VEGFR2 expression in endothelial cells was examined. The CTRP2 level associated with good collateral growth was observed in a cohort.
RESULTS
I/R reduced CTRP2 expression, and intraperitoneal injection of recombinant CTRP2 protein improved infarction size, cardiac function and angiogenesis. Overexpression of CTRP2 promoted blood refusion and collateral growth in ischaemic hindlimb mice. In vitro, CTRP2 enhanced tube formation and migration in a dose-dependent manner, while CTRP2 increased AKT phosphorylation and VEGFR2 expression. In an observational clinical cohort, CTRP2 levels were significantly increased in patients with good collateral growth, and CTRP2 was negatively associated with poor collateral growth in patients.
CONCLUSION
CTRP2 improved cardiac function by promoting collateral growth by promoting AKT-VEGFR2.
背景
侧支生长在急性心肌梗死的恢复中起着重要作用。C1q/TNF 相关蛋白-2（CTRP2）是 CTRP 家族的一员，对细胞存活表现出一些保护作用。在这项研究中，研究了 CTRP2 与侧支生长之间的关系。
方法
将 C57BL/6 小鼠进行心肌缺血/再灌注（I/R），并检测 CTRP2 的表达以及 CTRP2 对梗死面积、心脏功能和血管生成的影响。还使用缺血性后肢模型来检测 CTRP2 的作用。在体外，检测了 CTRP2 对血管生成、AKT 激活和血管内皮生长因子受体 2（VEGFR2）表达的调节作用。观察了与良好侧支生长相关的 CTRP2 水平。
结果
I/R 降低了 CTRP2 的表达，腹腔内注射重组 CTRP2 蛋白可改善梗死面积、心脏功能和血管生成。过表达 CTRP2 可促进缺血后肢小鼠的血液再灌注和侧支生长。在体外，CTRP2 以剂量依赖的方式增强管形成和迁移，同时 CTRP2 增加 AKT 磷酸化和 VEGFR2 表达。在观察性临床队列中，良好侧支生长患者的 CTRP2 水平显著升高，而 CTRP2 与患者侧支生长不良呈负相关。
结论
CTRP2 通过促进 AKT-VEGFR2 促进侧支生长来改善心脏功能。
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