The phenomenon of no-reflow seriously limits the therapeutic value of coronary recanalization and leads to poor prognosis. Recent studies have demonstrated the potential role of pigment epithelium-derived factor (PEDF) in stabilizing endothelial cell junction, reducing vascular permeability and maintaining a quiescent vasculature. In this study, intramyocardial gene delivery was performed 5 days before the acute myocardial infarction/recanalization experiment in male rats. Positron emission tomography perfusion imaging with ¹³N-NH₃ indicated PEDF to promote microvascular reperfusion significantly 4 h postcoronary occlusion. PEDF was observed to maintain the stability of endothelial adherens junctions (AJs), thus preventing the occurrence of no-reflow. PEDF reduced the hypoxia-induced vascular endothelial (VE)-cadherin endocytosis through PEDF/LR/Src/VE-cadherin S665 axis in vitro, which was remarkably observed to maintain endothelial AJs. Generally, PEDF might function as a relevant target for therapeutic vasculoprotection by way of regulating the phosphorylation level of VE-cadherin according to our data, thus being crucial for preventing no-reflow.

中文翻译：

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通过色素上皮衍生因子保持血管完整性来减轻心肌梗塞和无复流的策略

无复流现象严重限制了冠状动脉再通的治疗价值，导致预后不良。最近的研究表明色素上皮衍生因子 (PEDF) 在稳定内皮细胞连接、降低血管通透性和维持静止脉管系统方面的潜在作用。本研究在雄性大鼠急性心肌梗死/再通实验前5天进行心肌内基因递送。^使用13 N-NH ₃的正电子发射断层扫描灌注成像表明PEDF在冠状动脉闭塞后4小时显着促进微血管再灌注。观察到 PEDF 可维持内皮粘附连接 (AJ) 的稳定性，从而防止发生无回流。PEDF在体外通过 PEDF/LR/Src/VE-cadherin S665 轴减少缺氧诱导的血管内皮 (VE)-cadherin 内吞作用，显着观察到维持内皮 AJ。通常，根据我们的数据，PEDF 可能通过调节 VE-钙粘蛋白的磷酸化水平作为治疗性血管保护的相关靶点，因此对于防止无复流至关重要。