Objective To explore the function and mechanism of LncRNA Terc in endothelial-mesenchymal transition(End-MT)of human coronary artery endothelial cell(HCAEC).Methods The End-MT model of HCAEC was constructed by using transfor-ming growth factor-β(TGF-β)as inducer,LncRNA Terc knockdown or overexpression plasmid transfected cells,or combined with NOD-like receptor thermal protein domain associated protein 3(NLRP3)inflammasome inhibitor,nuclear factor-κB(NF-κB)inhib-itor intervention cells.The proliferation activity and migration ability of cells were detected by CCK-8 assay and Transwell assay.The ex-pression of inflammatory factors were detected by enzyme-linked immunosorbent assay(ELISA).The expressions of fibrosis-related proteins and inflammasome marker proteins were detected by Western blot.The expression level of lncRNA Terc was detected by real-time fluorescence quantitative polymerase chain reaction(RT-qPCR).Results LncRNA Terc was up-regulated in End-MT cell model(P＜0.01).After knockdown of LncRNA Terc,the proliferation activity and migration ability of HCAEC were significantly de-creased,and the expressions of alpha-smooth muscle actin(α-SMA),collagen Ⅰ and NLRP3 inflammatosomal marker proteins were significantly down-regulated,as well as the expressions of inflammatory factors IL-1β and IL-18(P＜0.01).However,the results after overexpression of lncRNA Terc were opposite.NLRP3 inflammasome inhibitors can weaken the induction effect of lncRNA Terc on End-MT.The addition of an NF-κB inhibitor resulted in a significantly down-regulation of NLRP3,caspase-1,apoptosis-associat-ed speck-like protein containing a CARD(ASC),IL-1 β and IL-18(P＜0.01).Conclusion LncRNA Terc can promote End-MT in HCAEC by regulating the NF-κB/NLRP3 pathway.

Objective To explore the function and mechanism of LncRNA Terc in endothelial-mesenchymal transition(End-MT)of human coronary artery endothelial cell(HCAEC).Methods The End-MT model of HCAEC was constructed by using transfor-ming growth factor-β(TGF-β)as inducer,LncRNA Terc knockdown or overexpression plasmid transfected cells,or combined with NOD-like receptor thermal protein domain associated protein 3(NLRP3)inflammasome inhibitor,nuclear factor-κB(NF-κB)inhib-itor intervention cells.The proliferation activity and migration ability of cells were detected by CCK-8 assay and Transwell assay.The ex-pression of inflammatory factors were detected by enzyme-linked immunosorbent assay(ELISA).The expressions of fibrosis-related proteins and inflammasome marker proteins were detected by Western blot.The expression level of lncRNA Terc was detected by real-time fluorescence quantitative polymerase chain reaction(RT-qPCR).Results LncRNA Terc was up-regulated in End-MT cell model(P＜0.01).After knockdown of LncRNA Terc,the proliferation activity and migration ability of HCAEC were significantly de-creased,and the expressions of alpha-smooth muscle actin(α-SMA),collagen Ⅰ and NLRP3 inflammatosomal marker proteins were significantly down-regulated,as well as the expressions of inflammatory factors IL-1β and IL-18(P＜0.01).However,the results after overexpression of lncRNA Terc were opposite.NLRP3 inflammasome inhibitors can weaken the induction effect of lncRNA Terc on End-MT.The addition of an NF-κB inhibitor resulted in a significantly down-regulation of NLRP3,caspase-1,apoptosis-associat-ed speck-like protein containing a CARD(ASC),IL-1 β and IL-18(P＜0.01).Conclusion LncRNA Terc can promote End-MT in HCAEC by regulating the NF-κB/NLRP3 pathway.