Linc01635对川崎病血管内皮细胞凋亡的影响

doi:10.3969/j.issn.2095-9400.2020.07.002

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Abstract Objective: To investigate the effect of linc01635 on apoptosis of vascular endothelial cells in Kawasaki disease (KD). Methods: Bioinformatics prediction and RNA FISH was employed to detect Subcellular localization of linc01635. Human umbilical vein endothelial cells (HUVECs) were cultured using KD plasma and healthy control plasma, qRT-PCR was used to detect the relative expression of linc01635 in HUVECs. Linc01635 expression in HUVECs was knocked-down by linc01635 siRNA and up-regulated by lentivirusor. Flow cytometry was used to analyze the apoptosis of HUVECs. Apoptosis was induced by KD plasma and the effect of linc01635 on KD-induced vascular endothelial cell injury was detected. Results: Linc01635 was distributed in both nuclei and cytoplasm of HUVECs. Compared with the healthy control group, KD plasma-treated HUVECs exhibited reduced expression of linc01635 (P<0.01). Overexpression of linc01635 inhibited HUVECs apoptosis (P<0.01), while knockdown of linc01635 increased HUVECs apoptosis (P<0.01). KD plasma could promote HUVECs apoptosis, and overexpression of linc01635 could inhibit KD plasma-induced apoptosis (P<0.01). Conclusion: KD plasma treatment can reduce the expression of linc01635 in vascular endothelial cells, which decreased linc01635 via KD plasma stimulation can induce vascular endothelial cells apoptosis.

Key words： Kawasaki disease vascular endothelial cells lncRNA linc01635

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	CHEN Ruiyao1
	RONG Xing
	WU Tingting
	JIA Chang
	WU Rongzhou
	CHU Maoping
	ZHANG Chunxiang

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https://xb.wmu.edu.cn/EN/10.3969/j.issn.2095-9400.2020.07.002 OR https://xb.wmu.edu.cn/EN/Y2020/V50/I7/525

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