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Mesenchymal stem cells alleviate experimental rheumatoid arthritis through microRNA-regulated IκB expression

Xin Yan1, Yurong Cen2, Qin Wang2,3

  • 1Department of Rheumatology, Shanxi University affiliated the First Hospital, Taiyuan 030001, China.

Scientific Reports
|June 30, 2016
PubMed

Insights

Mesenchymal stem cell (MSC) transplantation eases rheumatoid arthritis (RA) in mice by reducing NF-κB signaling. This occurs partly by suppressing microRNA-548e (miR-548e), which normally inhibits the NF-κB inhibitor IκB.

Area of Science:

  • Immunology
  • Stem Cell Biology
  • Molecular Biology

Background:

  • Mesenchymal stem cell (MSC) transplantation shows therapeutic potential in collagen-induced arthritis (CIA), a mouse model for human rheumatoid arthritis (RA).
  • The precise molecular mechanisms underlying MSC therapy for RA are not fully understood.

Purpose of the Study:

  • To elucidate the molecular pathways through which MSC transplantation exerts its therapeutic effects in a mouse model of RA.
  • To investigate the role of NF-κB signaling and microRNA-548e (miR-548e) in MSC-mediated amelioration of CIA.

Main Methods:

  • Utilized a collagen-induced arthritis (CIA) mouse model.
  • Assessed NF-κB signaling activity and miR-548e levels in joint tissues.
  • Employed bioinformatics to predict miR-548e targets.
  • Used adeno-associated virus (AAV) vectors to manipulate miR-548e levels in vivo.

Main Results:

  • MSC transplantation reduced NF-κB signaling activity and miR-548e levels in CIA mice.
  • miR-548e was predicted to inhibit the translation of IκB (an NF-κB inhibitor) mRNA.
  • Co-transplantation of MSCs with miR-548e-expressing AAV abolished therapeutic effects.
  • Transplantation of an miR-548e inhibitor (as-miR-548e) partially replicated MSC therapeutic effects.

Conclusions:

  • MSC transplantation may alleviate experimental RA partly by suppressing miR-548e.
  • Suppression of miR-548e leads to reduced inhibition of IκB, thereby dampening NF-κB signaling.
  • This study identifies a novel mechanism involving miR-548e in the immunomodulation of experimental arthritis by MSCs.

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