OIP5-AS1 facilitates Th17 differentiation and EAE severity by targeting miR-140-5p to regulate RhoA/ROCK2 signaling

Ruihua Liu1, Yan Li1, Haitao Zhou1

  • 1Department of Neurology, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, China.

Life Sciences
|January 30, 2021
PubMed
Abstract

Insights

Long non-coding RNA OIP5-AS1 promotes multiple sclerosis (MS) development by enhancing T-helper 17 cell differentiation via the miR-140-5p/RhoA pathway. This study reveals OIP5-AS1 as a potential therapeutic target for MS.

Area of Science:

  • Neuroimmunology
  • Molecular Biology
  • Genetics

Background:

  • Multiple sclerosis (MS) is a common neurological disorder with complex etiology.
  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in autoimmune diseases.
  • OIP5-AS1 has been implicated in the pathogenesis of MS.

Purpose of the Study:

  • To investigate the role of lncRNA OIP5-AS1 in the development of MS.
  • To elucidate the molecular mechanisms underlying OIP5-AS1's function in MS pathogenesis.
  • To explore OIP5-AS1 as a potential therapeutic target for MS.

Main Methods:

  • Quantitative real-time PCR (RT-qPCR) to measure gene expression.
  • Flow cytometry to analyze T-helper 17 (Th17) cell populations.
  • Luciferase reporter assays to validate molecular interactions.
  • Experimental autoimmune encephalomyelitis (EAE) mouse model to study MS in vivo.

Main Results:

  • OIP5-AS1 expression is upregulated in MS patients and during Th17 cell differentiation.
  • OIP5-AS1 promotes Th17 differentiation in vitro and exacerbates EAE in vivo.
  • OIP5-AS1 targets miR-140-5p, which in turn regulates the RhoA/ROCK2 signaling pathway.
  • RhoA upregulation counteracts the inhibitory effects of miR-140-5p on Th17 differentiation.

Conclusions:

  • OIP5-AS1 plays a critical role in MS pathogenesis by promoting Th17 cell differentiation.
  • The OIP5-AS1/miR-140-5p/RhoA axis is a key molecular mechanism in MS development.
  • OIP5-AS1 represents a potential diagnostic and therapeutic target for multiple sclerosis.

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