Depletion of miR-155 hinders the myofibroblast activities and reactive oxygen species generation in oral submucous fibrosis

Ming Yung Chou, Chih Yuan Fang, Pei Ling Hsieh, Yi Wen Liao, Cheng Chia Yu, Shiuan Shinn Lee

Research output: Contribution to journalArticlepeer-review

Abstract

Background/purpose: Emerging evidence suggests the significance of microRNA-155 (miR-155) in fibrogenesis and oxidative stress accumulation, but its function in oral submucous fibrosis (OSF) has not been investigated. In this study, we assessed the expression of miR-155 and its effects on the maintenance of myofibroblast activation. Methods: qRT-PCR was conducted to assess the expression of miR-155 in OSF tissues and fibrotic buccal mucosal fibroblasts (fBMFs) derived from OSF samples. Collagen gel contraction, migration, and invasion capabilities were examined in fBMFs. DCFDA ROS assay was used to examine ROS generation. A luciferase reporter assay was carried out to verify the relationship between miR-155 and its potential target RPTOR. Results: We showed that the expression of miR-155 was aberrantly upregulated in OSF specimens and fBMFs. Inhibition of miR-155 ameliorated various myofibroblast activities, including collagen gel contraction, migration, and invasion abilities as well as ROS production. Results from the luciferase reporter assay demonstrated that miR-155 directly interacted with its target RPTOR. Conclusion: Taken together, these findings indicate that miR-155 is implicated in the pathogenesis of oxidative stress-associated OSF, possibly through the regulation of RPTOR.

Original languageEnglish
JournalJournal of the Formosan Medical Association
DOIs
Publication statusAccepted/In press - 2021

Keywords

  • miR-155
  • Myofibroblast
  • Oral submucous fibrosis

ASJC Scopus subject areas

  • Medicine(all)

Fingerprint

Dive into the research topics of 'Depletion of miR-155 hinders the myofibroblast activities and reactive oxygen species generation in oral submucous fibrosis'. Together they form a unique fingerprint.

Cite this