Related Experiment Video
Updated: Nov 19, 2025

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
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.
Aims:
Multiple sclerosis (MS) is one of the commonest neurologic disorders globally. LncRNA OIP5-AS1 has been found to be implicated in the etiology of MS. This study was to explore the roles and molecular mechanisms of OIP5-AS1 in the development of MS.
Materials And Methods:
RT-qPCR assay was used to measure expressions of OIP5-AS1, miR-140-5p, IL-17A mRNA and RhoA mRNA. CD4+IL-17+ cell proportion was determined by flow cytometry. IL-17A secretion was examined by ELISA assay. Cell inflammatory infiltration and demyelination were assessed by histological analyses. The interaction between miR-140-5p and OIP5-AS1 or RhoA 3'UTR was validated by bioinformatical analysis and luciferase reporter assay. Western blot assay was performed to detect protein expressions of ROCK2 and RhoA. An experimental autoimmune encephalomyelitis (EAE) models was established to explore the role of OIP5-AS1 in MS in vivo.
Key Findings:
OIP5-AS1 expression was enhanced in MS patients. Also, elevated OIP5-AS1 level was observed during T-helper 17 (Th17) differentiation. Moreover, OIP5-AS1 promoted Th17 differentiation in vitro and contributed to the development of EAE in vivo. Mechanical explorations revealed that OIP5-AS1 targeted miR-140-5p to regulate Th17 differentiation. Moreover, RhoA was a target of miR-140-5p and miR-140-5p inhibited the activation of RhoA/ROCK2 signaling. Also, RhoA upregulation abrogated the inhibitory effects of miR-140-5p on Th17 differentiation.
Significance:
OIP5-AS1 contributed to EAE development by targeting miR-140-5p/RhoA and activating RhoA/ROCK2 signaling pathway, shedding light on the roles and molecular mechanisms of OIP5-AS1 in the development of MS and providing some candidate targets for the diagnose and treatment of MS.
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.
More Related Videos
Related Concept Videos
T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
IP3/DAG Signaling Pathway
The JAK-STAT Signaling Pathway
TGF - β Signaling Pathway
EPS and iPS Cells in Disease Research
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

