microRNA‐491‐5p regulates osteogenic differentiation of bone marrow stem cells in type 2 diabetes
Objectives Osseointegration of oral implants has a low success rate in patients with type 2 diabetes. This is because of the inhibition of osteogenic differentiation in the jawbone marrow mesenchymal stem cells, in which the expression of microRNA(miR)‐491‐5p is significantly downregulated, as ascer...
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Published in | Oral diseases Vol. 29; no. 1; pp. 308 - 321 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Denmark
Wiley Subscription Services, Inc
01.01.2023
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Subjects | |
Online Access | Get full text |
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Summary: | Objectives
Osseointegration of oral implants has a low success rate in patients with type 2 diabetes. This is because of the inhibition of osteogenic differentiation in the jawbone marrow mesenchymal stem cells, in which the expression of microRNA(miR)‐491‐5p is significantly downregulated, as ascertained through gene chip screening. However, the underlying mechanisms are unclear. Here, we aimed to clarify the mechanisms involved in the influence of miR‐491‐5p on osteogenic differentiation.
Subjects and methods: Jawbone marrow mesenchymal stem cells were isolated from jawbones of patients with type 2 diabetes and subjected to bioinformatics and functional analyses. Osteogenesis experiments were conducted using the isolated cells and an in vivo model.
Results
Knockdown and overexpression experiments revealed the positive effects of miR‐491‐5p expression on osteogenic differentiation in vivo and in vitro. Additionally, a dual‐luciferase assay revealed that miR‐491‐5p targeted the SMAD/RUNX2 pathway by inhibiting the expression of epidermal growth factor receptor.
Conclusions
miR‐491‐5p is vital in osteogenic differentiation of jawbone mesenchymal stem cells; its downregulation in type 2 diabetes could be a major cause of decreased osteogenic differentiation. Regulation of miR‐491‐5p expression could improve osteogenic differentiation of jawbone mesenchymal stem cells in patients with type 2 diabetes. |
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Bibliography: | Funding information This research was funded by the National Natural Science Foundation of China, grant No. 81371115 to Jun Li ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
ISSN: | 1354-523X 1601-0825 1601-0825 |
DOI: | 10.1111/odi.14005 |