Evodiamine-Mediated Effects of miR-223-3p on the Proliferation, Migration and Angiogenesis of Myocardial Microvascular Endothelial Cells
LIU Wenpin, XIONG Xianghui*, MAO Xiangping
To investigate the mechanism of Evodiamine-mediated miR-223-3p on the proliferation, migration and angiogenesis of myocardial microvascular endothelial cells induced by hypoxia, rat myocardial microvascular endothelial cells were isolated and cultured in vitro in this study. The cells were divided into control group (Con), hypoxia group (Hypoxia), low, medium, and high dose evodiamine groups (Evodiamine-L, M, H), anti-miRNC group, anti-miR-223-3p group, Evodiamine+miR-NC group (Evodiamine+miR-NC), Evodiamine+miR-223- 3p group (Evodiamine+miR-223-3p). The other groups were all treated with hypoxia except for the Con group. MTT was used to detect cell proliferation changes; Transwell test was used to detect cell migration ability; Western blot was used to detect VEGF protein expression; angiogenesis test was used to detect blood vessel formation; RT-qPCR was used to detect miR-223-3p expression level. The results show that, the cell activity, the number of migration cells of Hypoxia group were significantly lower than those of Con group (P<0.05), and the VEGF protein expression, angiogenesis length, and miR-223-3p expression levels were significantly higher than those of Con group (P<0.05). The cell viability, number of migration cells, VEGF protein expression, and angiogenesis length of Evodiamine-L, Evodiamine-M, and Evodiamine-H groups were significantly higher than those of Hypoxia group (P<0.05), and the expression level of miR-223-3p was significantly lower than that of Hypoxia group (P<0.05). The expression level of miR-223-3p in the anti-miR-223-3p group was significantly lower than that in the anti-miRNC group (P<0.05), and the cell activity, number of migration cells, VEGF protein expression, and angiogenesis length in the anti-miR-223-3p group were significantly higher than those in the anti-miR-NC group (P<0.05). The expression level of miR-223-3p in the Evodiamine+miR-223-3p group was significantly higher than that in the Evodiamine+miR-NC group (P<0.05), and the cell activity, number of migration cells, VEGF protein expression, and angiogenesis length were significantly lower than those in the Evodiamine+miR-NC group (P<0.05). These aforementioned findings indicates that evodiline may promote hypoxia-induced myocardial microvascular endothelial cell proliferation, migration and angiogenesis by down-regulating miR-223-3p.
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