Upregulation of miR-23b Enhances the Autologous Therapeutic Potential for Degenerative Arthritis by Targeting PRKACB in Synovial Fluid-Derived Mesenchymal Stem Cells from Patients

The use of synovial fluid-derived mesenchymal stem cells (SFMSCs) obtained from patients with degenerative arthropathy may serve as an alternative therapeutic strategy in osteoarthritis (OA) and rheumatoid arthritis (RA). For treatment of OA and RA patients, autologous transplantation of differentia...

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Published inMolecules and cells Vol. 37; no. 6; pp. 449 - 456
Main Authors Ham, Onju, Lee, Chang Youn, Song, Byeong-Wook, Lee, Se-Yeon, Kim, Ran, Park, Jun-Hee, Lee, Jiyun, Seo, Hyang-Hee, Lee, Chae Yoon, Chung, Yong-An, Maeng, Lee-So, Lee, Min Young, Kim, Jongmin, Hwang, Jihwan, Woo, Dong Kyun, Chang, Woochul
Format Journal Article
LanguageEnglish
Published United States Korean Society for Molecular and Cellular Biology 01.06.2014
한국분자세포생물학회
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ISSN1016-8478
0219-1032
DOI10.14348/molcells.2014.0023

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Summary:The use of synovial fluid-derived mesenchymal stem cells (SFMSCs) obtained from patients with degenerative arthropathy may serve as an alternative therapeutic strategy in osteoarthritis (OA) and rheumatoid arthritis (RA). For treatment of OA and RA patients, autologous transplantation of differentiated MSCs has several beneficial effects for cartilage regeneration including immunomodulatory activity. In this study, we induced chondrogenic differentiation of SFMSCs by inhibiting protein kinase A (PKA) with a small molecule and microRNA (miRNA). Chondrogenic differentiation was confirmed by PCR and immunocytochemistry using probes specific for aggrecan, the major cartilaginous proteoglycan gene. Absorbance of alcian blue stain to detect chondrogenic differentiation was increased in H-89 and/or miRNA-23btransfected cells. Furthermore, expression of matrix metalloproteinase (MMP)-9 and MMP-2 was decreased in treated cells. Therefore, differentiation of SFMSCs into chondrocytes through inhibition of PKA signaling may be a therapeutic option for OA or RA patients.
Bibliography:These authors contributed equally to this work.
http://dx.doi.org/10.14348/molcells.2014.0023
G704-000079.2014.37.6.001
ISSN:1016-8478
0219-1032
DOI:10.14348/molcells.2014.0023