Effects Of Long Non-coding LncRNA DBH-AS1 On The Apoptosis Of Keloid Fibroblasts And Its Mechanism

ObjectiveTo explore the effect and mechanism of long non-coding RNA DBH-A S1(DBH-AS1)on the apoptosis of keloid fibroblasts to analyze its mecha nism.MethodsReal-time fluorescent quantitative reverse transcription polymerase chain reaction(q RT-PCR)was used to detect DBH-AS1,micro RNA-138(mi R-138)and Hypoxia-inducible factor-1α(HIF-1α)m RNA expression levels in keloids and normal skin tissues.Dual luciferase assay was applied to analyze the binding of DBH-AS1 and mi R-138,and mi R-138 and HIF-1α.After fibroblasts transfected with sh-DBH-AS1,LV-mi R-138,sh-mi R-138,and sh-HIF-1αrespectively,the cell apoptosis was detected by flow cytometry;the expression changes of mi R-138 and HIF-1α were detected by Western blot and RT-PCR.ResultsThe expression levels of DBH-AS1 and HIF-1α in keloid tissues were significantly higher than those in normal skin(P<0.05).The expression level of mi R-138 in keloid tissues was lower than that in normal skin(P<0.05).The Dual Luciferase Report verified that DBH-AS1 could target mi R-138,and mi R-138 could target HIF-1α in keloid fibroblast.Besides,low expression of DBH-AS1 or overexpression of mi R-138 significantly promoted the apoptosis of keloid fibroblasts.Knockdown of mi R-138 could reverse the effect of silencing DBH-AS1 on the apoptosis of keloid fibroblasts,but further accelerated the inhibitory effect of overexpression DBH-AS1 on the apoptosis of keloid fibroblasts.Knockdown of HIF-1α significantly reversed the effect of silencing mi R-138 on apoptosis,increased the promotion effect of mi R-138 overexpression on apoptosis(P<0.05).ConclusionsDBH-AS1 was highly expressed in keloid tissue,down-regulated of DBH-AS1 could promote the apoptosis of keloid fibroblasts by regulating the mi R-138/ HIF-1α pathway,suggesting that DBH-AS1 may become a potential target for the treatment of keloids.