PEDF Improves Cardiac Function in Rats with Acute Myocardial Infarction via Inhibiting Vascular Permeability and Cardiomyocyte Apoptosis

International Journal of Molecular Sciences

Hao Zhang²  Zheng Wang²  Shou-Jie Feng²  Lei Xu²  He-Xian Shi²  Li-Li Chen²  Guang-Da Yuan²  Wei Yan²  Wei Zhuang¹  Yi-Qian Zhang²  Zhong-Ming Zhang²  Hong-Yan Dong¹ 

[1] Research Facility Center for Morphology, Xuzhou Medical College, Xuzhou 221004, China; E-Mail:;Department of Thoracic Cardiovascular Surgery, Affiliated Hospital of Xuzhou Medical College, Xuzhou 221006, China; E-Mails:

关键词: pigment epithelium-derived factor (PEDF);    myocardial infarction;    cardiac function;    vascular permeability;    PPARγ;    apoptosis;   

DOI  :  10.3390/ijms16035618

来源: mdpi

【 摘 要 】

Pigment epithelium-derived factor (PEDF) is a pleiotropic gene with anti-inflammatory, antioxidant and anti-angiogenic properties. However, recent reports about the effects of PEDF on cardiomyocytes are controversial, and it is not known whether and how PEDF acts to inhibit hypoxic or ischemic endothelial injury in the heart. In the present study, adult Sprague-Dawley rat models of acute myocardial infarction (AMI) were surgically established. PEDF-small interfering RNA (siRNA)-lentivirus (PEDF-RNAi-LV) or PEDF-LV was delivered into the myocardium along the infarct border to knockdown or overexpress PEDF, respectively. Vascular permeability, cardiomyocyte apoptosis, myocardial infarct size and animal cardiac function were analyzed. We also evaluated PEDF’s effect on the suppression of the endothelial permeability and cardiomyocyte apoptosis under hypoxia in vitro. The results indicated that PEDF significantly suppressed the vascular permeability and inhibited hypoxia-induced endothelial permeability through PPARγ-dependent tight junction (TJ) production. PEDF protected cardiomyocytes against ischemia or hypoxia-induced cell apoptosis both in vivo and in vitro via preventing the activation of caspase-3. We also found that PEDF significantly reduced myocardial infarct size and enhanced cardiac function in rats with AMI. These data suggest that PEDF could protect cardiac function from ischemic injury, at least by means of reducing vascular permeability, cardiomyocyte apoptosis and myocardial infarct size.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.