The Journal of Practical Medicine ›› 2021, Vol. 37 ›› Issue (2): 226-232.doi: 10.3969/j.issn.1006⁃5725.2021.02.019

• Clinical Research • Previous Articles     Next Articles

Impact of long non⁃coding lncRNA DBH⁃AS1 on apoptosis of keloid fibroblasts and its mechanism of action

JIA Chunying,ZHANG Rongming
  

  1. Department of Burn and Plastic Surgery,Affiliated Third Hospital,Jin⁃zhou Medical University,Jinzhou 121000,China
  • Online:2021-01-25 Published:2021-01-25
  • Contact: ZHANG Rongming E⁃mail:zrm99999@126.com

Abstract:

Objective To explore the effect of long non⁃coding lncRNA DBH⁃AS1(DBH⁃AS1)on apoptosis of keloid fibroblasts and its mechanism of action. Methods Real⁃time fluorescent quantitative reverse transcription polymerase chain reaction(qRT⁃PCR)was used to detect mRNA expression levels of DBH⁃AS1,microRNA⁃138 (miR⁃138)and Hypoxia⁃inducible factor⁃1α(HIF⁃1α)in keloids and normal skin tissues. Dual Luciferase Report was applied to analyze the combination of the three proteins. Flow cytometry,qRT ⁃PCR and Western blot were utilized to detect the effect of knockdown or overexpression of DBH⁃AS1 on apoptosis of keloid fibroblasts,the expression changes of miR⁃138 and HIF⁃1α were also analyzed. Results DBH⁃AS1 and HIF⁃1α were significantly up⁃regulated in keloid tissues and cells while miR⁃138 was significantly down⁃regulated(P < 0.05). The Dual Lucif⁃ erase Report verified that DBH⁃AS1 could have targeted binding with miR⁃138,and miR⁃138 could have targeted binding with HIF⁃1α in keloid fibroblast. Low expression of DBH⁃AS1 or overexpression of miR⁃138 significantly promoted apoptosis of keloid fibroblasts. Knockdown of miR⁃138 could reverse the effect of silencing DBH⁃AS1 on apoptosis of keloid fibroblasts,and knockdown of HIF⁃1α significantly inhibited the effect of silencing miR⁃138 on apoptosis(P < 0.05). Conclusions Silencing DBH⁃AS1 promoted apoptosis of keloid fibroblasts by regulating the miR⁃138/HIF⁃1α pathway,

Key words: