|
|
|
| The effect of antagomir-30d on osteogenic differentiation of bone mesenchymal stem cells |
| WANG Yan1, JIN Qiong1, CHEN Wei2, HUANG Hui3 |
| 1.Department of Implant Prosthodontics, School & Hospital of Stomatology, Wenzhou Medical University, Wenzhou 325027, China; 2.Department of Pediatric Dentistry, School & Hospital of Stomatology, Wenzhou Medical University, Wenzhou 325027, China; 3.Department of Prosthodontics, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China |
|
| Cite this article: |
|
WANG Yan,JIN Qiong,CHEN Wei, et al. The effect of antagomir-30d on osteogenic differentiation of bone mesenchymal stem cells[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2021, 51(6): 478-482.
|
|
|
|
Abstract Objective: To verify the upregulating effect of antagomir-30d (miR-30d) on osteogenic differentiation of bone mesenchymal stem cells (BMSCs) and to confirm the optimum transfection concentration. Methods: Antagomir-30d of different concentrations was divided into antagomir-30d (antagomir-30d group), negative control (NC group) and untransfected BMSCs (blank group). Transfecting different concentrations of antagomir-30d/NC/blank to BMSCs, gene expression of osteoblast marker genes (ALP, OC and RUNX2) was analyzed using RT-PCR and then optimum transfection concentration and transfection efficiency were confirmed. The role of antagomir-30d in regulating osteogenesis was verified by ALP staining. Results: The results of RT-PCR showed that antagomir-30d enhanced osteogenic differentiation of BMSCs in vitro. The transfection effect changed according to transfection concentration. When transfected with 150 nmol/L, the expression of ALP, OC and RUNX2 in the antagomir-30d group was significantly higher than the other groups. Meanwhile, there was no significant change in the proliferation and apoptosis of BMSCs when transfected with 150 nmol/L. Therefore, 150 nmol/L proved to be optimum ALP staining showed ALP activity of antagomir-30d group was significantly upregulated. Conclusion: The antagonist of miR-30d (antagomir-30d) promotes osteogenic differentiation of BMSCs in vitro and 150 nmol/L is the optimum transfected concentration.
|
|
Received: 03 September 2020
|
| |
|
|
|
参考文献：
[1] LU T X, ROTHENBERG M E. MicroRNA[J]. J Allergy Clin Immunol, 2018, 141(4): 1202-1207.
[2] WU T, ZHOU H, HONG Y, et al. MiR-30 family members negatively regulate osteoblast differentiation[J]. J Biol Chem, 2012, 287(10): 7503-7511.
[3] CROSET M, PANTANO F, KAN C W S, et al. MiRNA-30 family members inhibit breast cancer invasion, osteomimicry, and bone destruction by directly targeting multiple bone metastasis-associated genes[J]. Cancer Res, 2018, 78(18): 5259-5273.
[4] LI Z, HASSAN M Q, VOLINIA S, et al. A microRNA signature for a BMP2-induced osteoblast lineage commitment program[J]. Proc Natl Acad Sci U S A, 2008, 105(37): 13906-13911.
[5] OWEN M. Marrow stromal stem cells[J]. J Cell Sci Suppl, 1988, 10: 63-76.
[6] MAUNEY J R, VOLLOCH V, KAPLAN D L. Role of adult mesenchymal stem cells in bone tissue engineering applications: Current status and future prospects[J]. Tissue Eng, 2005, 11(5-6): 787-802.
[7] MARTIN T J, SIMS N A. Osteoclast-derived activity in the coupling of bone formation to resorption[J]. Trends Mol Med, 2005, 11(2): 76-81.
[8] FRANCESCHI R T, GE C, XIAO G, et al. Transcriptional regulation of osteoblasts[J]. Ann N Y Acad Sci, 2007, 1116: 196-207.
[9] POPOVIC R, RIESBECK L E, VELU C S, et al. Regulation of mir-196b by MLL and its overexpression by MLL fusions contributes to immortalization[J]. Blood, 2009, 113(14): 3314-3322.
[10] DING Y, WU M, LIU J, et al. Seed-targeting anti-miR-21 inhibiting malignant progression of retinoblastoma and analysis of their phosphorylation signaling pathways[J]. Exp Eye Res, 2014, 122: 1-8.
[11] 李奇, 杨俊, 杨简, 等. 大鼠microRNA-327重组腺病毒载体的构建及其在心肌细胞的转染效率[J]. 解剖学杂志, 2019, 42(3): 244-248. |
| [1] |
. [J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2021, 51(12): 1020-1024. |
|
|
|
|
