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目的 观察骨桥蛋白(OPN)转基因小鼠(OPN-/- )心肌梗死后心肌血管新生能力及其与左室重构的关系。方法 采用OPN-/-小鼠体外心肌内皮细胞管结构形成、体内心肌Matrigel植入及心肌梗死3 种模型,以野生型小鼠(WT)作为对照。结果 体外培养的OPN-/- 小鼠心肌血管内皮细胞在Matrigel的管结构生成显著减弱,可溶性OPN能明显改善OPN-/- 内皮细胞的管结构生成能力。在OPN-/- 小鼠心肌Matrigel植入模型,毛细血管样结构生成的体积明显降低。OPN-/-小鼠心肌梗死后7和14 d,梗死区毛细血管密度和小动脉密度均明显降低。且在梗死后7~14 d,OPN / 小鼠小动脉的去血管化速率显著加快。OPN-/-小鼠心肌梗死后,左室扩大及梗死区室壁变薄均较对照组显著。结论 OPN的促血管新生机制在心肌梗死后左室重构的调节中起重要作用。
Objective To investigate the relationship between myocardial angiogenesis and left ventricular remodeling after osteopontin (OPN) transgenic mice (OPN - / -) myocardial infarction. Methods Three kinds of models of myocardial endothelial cell tube structure formation, intramyocardial Matrigel implantation and myocardial infarction in OPN - / - mice were used, and wild type mice (WT) were used as control. Results The vascular endothelial cells of OPN - / - mice cultured in vitro were significantly reduced in the tube structure of Matrigel. Soluble OPN could significantly improve the tube formation ability of OPN - / - endothelial cells. In the Matrigel implanted model of OPN - / - mice, the volume of capillaries-like structures was significantly reduced. In the OPN - / - mice at 7 and 14 d after myocardial infarction, capillary density and arteriolar density were significantly decreased in the infarct zone. And in 7 ~ 14 d after infarction, OPN / mouse arteriolar de-vascularization rate significantly accelerated. OPN - / - mice after myocardial infarction, left ventricular enlargement and infarct wall thinning were significantly more than the control group. Conclusion The angiogenesis mechanism of OPN plays an important role in the regulation of left ventricular remodeling after myocardial infarction.