Lymphoangiocrine signal Hspg2 improves hypoxia/reoxygenation-induced endothelial dysfunction through PI3K/AKT pathway
Objective:To investigate the effect and mechanism of lymphoangiocrine signal heparan sulfate proteoglycan 2(Hspg2)on hypoxia/reoxygenation(H/R)-induced dysfunction of human umbilical vein endothelial cells(HUVECs).Methods:HUVECs were divided into the control group,H/R group,H/R+Hspg2 group,and H/R+Hspg2+LY294002(PI3K inhibitor)group.qRT-PCR was used to detect the level of Hspg2 mRNA in H/R cells;Nitric oxide(NO)assay kit was used to detect NO pro-duction;Western Blot was used to detect the expression of endothelial injury-related proteins(eNOS,ICAM-1,and VCAM-1),inflammasomes(NLRP3 and Caspase-1),and PI3K/AKT pathway related proteins.Results:The mRNA level of Hspg2 in H/R was significantly higher than that in normal cells.Compared with the H/R group,Hspg2 treatment significantly increased NO production and eNOS protein expression.The levels of ICAM-1,VCAM-1,NLRP3,and Caspase-1 proteins were significantly reduced,while the protein expression levels of p-PI3K/PI3K and p-AKT/AKT were sig-nificantly increased.Inhibition of the PI3K/AKT pathway significantly weakened the protective effect of Hspg2 on H/R-induced endothelial dysfunction.Conclusion:Hspg2 improves H/R-induced HU-VECs dysfunction by activating the PI3K/AKT signaling pathway.
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