Wang Dinghui, Liu Bin, Xiong Tianhua, Yu Wenlong, Yang Huiping, Wang Jing, Jing Xiaodong, She Qiang
Department of Cardiology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Cell Death Discov. 2022 Sep 10;8(1):381. doi: 10.1038/s41420-022-01180-5.
Forkhead box protein P1 (FoxP1) is essential for cardiac development and the regulation of neovascularization, but its potential for cardiac angiogenesis has not been explored. This study aims to investigate the angiogenic role of FoxP1 in a rat model of myocardial infarction (MI). Adult male rats were subjected to MI, and Foxp1 was knocked down with lentivirus FoxP1 siRNA. Endothelial cell proliferation, angiogenesis, and cardiac function were also assessed. Cell scratch assay and tubule formation analysis were used to detect the migration ability and tube formation ability of human umbilical vein endothelial cells (HUVECs). Compared with that in the sham group, results showed that the expression of FoxP1 was significantly increased in the MI group. Foxp1 knockdown decreases FoxP1 expression, reduces angiogenesis, and increases collagen deposition. When Foxp1 was knocked down in HUVECs using FoxP1 siRNA lentivirus, cell proliferation, migration, and tube formation abilities decreased significantly. Our study showed that FoxP1 elicits pleiotropic beneficial actions on angiogenesis in the post-MI heart by promoting the proliferation of endothelial cells. FoxP1 should be considered a candidate for therapeutic cardiac angiogenesis.
叉头框蛋白P1（FoxP1）对心脏发育和新生血管形成的调节至关重要，但其在心脏血管生成方面的潜力尚未得到探索。本研究旨在探讨FoxP1在大鼠心肌梗死（MI）模型中的血管生成作用。对成年雄性大鼠进行MI手术，并用慢病毒FoxP1小干扰RNA敲低Foxp1。同时评估内皮细胞增殖、血管生成和心脏功能。采用细胞划痕试验和小管形成分析检测人脐静脉内皮细胞（HUVECs）的迁移能力和管形成能力。结果显示，与假手术组相比，MI组中FoxP1的表达显著增加。敲低Foxp1可降低FoxP1表达，减少血管生成，并增加胶原沉积。当使用FoxP1小干扰RNA慢病毒在HUVECs中敲低Foxp1时，细胞增殖、迁移和管形成能力显著下降。我们的研究表明，FoxP1通过促进内皮细胞增殖，对MI后心脏的血管生成产生多效性有益作用。FoxP1应被视为治疗性心脏血管生成的候选因子。
