科研之友
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摘要
Objective: To investigate the expression level and mechanism of action of micro ribonucleic acid-214 (miR-214) during fracture healing, and to provide new clues and theoretical basis for the clinical treatment of nonunion. Methods: The expression of miR-214 in human mesenchymal stem cells (hMSCs) at different time points was detected via quantitative reverse transcription-polymerase chain reaction. miR-214 inhibitor and mimics were artificially synthesized and transfected to verify the role of miR-214 in osteogenic differentiation and chondrogenic differentiation. Osteogenic differentiation of hMSCs was induced using osteogenic induction culture solution to observe the expression of miR-214, runt-related transcription factor 2 (Runx2), alpha-1 type I collagen (COL1A1), and osteocalcin genes during osteogenic differentiation of hMSCs. Chondrogenic differentiation was induced using chondrogenic induction culture solution to observe expression of miR-214, alpha-1 type II collagen (COL2A1), aggrecan, and SOX9. Moreover, the rat model of femoral fracture was established, miR-214 control, miR-214 inhibitor, and miR-214 mimics were injected into the fracture end, and micro-CT images were observed after 8 weeks. Results: miR-214 was poorly expressed during osteogenic differentiation of hMSCs, and its expression level was decreased with time during induced differentiation. Inhibiting miR-214 expression could promote osteogenic differentiation, and expression of Runx2, COL1A1 and osteocalcin genes were up-regulated. Overexpression of miR214 expression could inhibit osteogenic differentiation, and expression of Runx2, COL1A1, and osteocalcin genes were inhibited. Inhibiting miR-214 expression could also promote chondrogenic differentiation, and expression of COL2A1, aggrecan, and SOX9 were up-regulated. Furthermore, injecting miR-214 inhibitor into the fracture end of rats could promote fracture healing and avoid the occurrence of nonunion. Conclusion: Inhibiting miR-214 expression can increase the fracture healing rate and reduce the incidence rate of nonunion, providing new therapeutic regimens for nonunion in clinical orthopedics.
