MiR-181a regulates the chondrogenic differentiation in pig peripheral blood mesenchymal stem cells
Articular cartilage injury and therapy are important clinical issues around the world. Mesenchymal stem cells (MSCs) have the ability to differentiate into chondrocytes, which makes MSCs good candidates for use in cartilage repairing. However the regulation and the mechanism of chondrogenesisin MSCs...
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Published in | International journal of clinical and experimental pathology Vol. 11; no. 2; pp. 947 - 955 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
e-Century Publishing Corporation
01.01.2018
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Subjects | |
Online Access | Get full text |
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Summary: | Articular cartilage injury and therapy are important clinical issues around the world. Mesenchymal stem cells (MSCs) have the ability to differentiate into chondrocytes, which makes MSCs good candidates for use in cartilage repairing. However the regulation and the mechanism of chondrogenesisin MSCs is still unclear. To clarify the factor and mechanism which contribute to the process of chondrogenic differentiation, we focus on miRNAs. Considering the role of miR-181a in chondrogenesis and osteoblast formation, we tested the expression of miR-181a in the induced chondrogenic differential pig PBMSCs by using qRT-PCR. And we identified miR-181a as an up-regulated miRNA in the TGF-β3-induced pig PBMSCs chondrogenic differentiation from the early stages and maintained elevated throughout the whole process. After inhibition of the endogenesis miR-181a expression by transfecting the miR-181a inhibitor, the western-blot results and immunofluorescence results indicated that the expression of differentiation-related protein COL2A1, BMP2 were decreased, together with the Alcian blue assay, proving the process of differentiation was inhibited significantly. Taken together, our results demonstrated that miR-181a might be necessary in chondrogenesis of MSCs. Even so, the mechanism of miR-181a on regulating the chondrogenesis still needed to be investigated in future work. And our data would provide an experimental evidence for the research of tissue engineering. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1936-2625 |