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Effect of miR-137 on the proliferation and apoptosis of endothelial cells regulated by AKT2 gene / 中华医学遗传学杂志
Article en Zh | WPRIM | ID: wpr-796460
Biblioteca responsable: WPRO
ABSTRACT
Objective@#To assess the effect of miR-137 on the proliferation and apoptosis of human umbilical vein endothelial cells (HUVECs) induced by high glucose and its mechanism.@*Methods@#HUVECs cells were divided into low-glucose group (5.5 mmol/L glucose-treated cells), high-glucose group (33.36 mmol/L glucose-treated cells), anti-NC group (cells treated with 33.36 mmol/L glucose after anti-NC transfection) and anti-miR-137 group (cells treated with 33.36 mmol/L glucose after anti-miR-137 transfection). After 48 hours, qRT-PCR was used to determine the expression of miR-137. CCK-8 assay and flow cytometry were used to detect cell proliferation and apoptosis rate, respectively. The targeting relationship between miR-137 and AKT2 was validated by dual fluorescence reporter gene detection system and AKT2 protein expression after overexpression or inhibition of miR-137.@*Results@#High glucose could significantly up-regulate the expression of miR-137 in HUVECs cells, and the expression of miR-137 in HUVECs cells transfected with miR-137 inhibitor was significantly decreased (P<0.05). High glucose can significantly inhibit HUVECs cell proliferation and induce apoptosis, while inhibition of miR-137 expression can weaken the effect of high glucose on HUVECs cell proliferation inhibition and apoptosis promotion (P<0.05). Inhibiting AKT2 expression could weaken the inhibitory effect of miR-137 inhibitor on HUVECs cell proliferation and apoptosis (P<0.05).@*Conclusion@#Inhibiting the expression of miR-137 gene can attenuate the proliferation inhibition and apoptosis promotion of HUVECs induced by high glucose, and the mechanism is related to activating the expression of AKT2.
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Texto completo: 1 Índice: WPRIM Idioma: Zh Revista: Zhonghua Yi Xue Yi Chuan Xue Za Zhi Año: 2019 Tipo del documento: Article
Texto completo: 1 Índice: WPRIM Idioma: Zh Revista: Zhonghua Yi Xue Yi Chuan Xue Za Zhi Año: 2019 Tipo del documento: Article