| Autor: |
LIAO Chunhui, LI Mingfei, YE Jinmei, PENG Wei, CHEN Songling |
| Jazyk: |
čínština |
| Rok vydání: |
2020 |
| Předmět: |
|
| Zdroj: |
口腔疾病防治, Vol 28, Iss 1, Pp 16-23 (2020) |
| Druh dokumentu: |
article |
| ISSN: |
2096-1456 |
| DOI: |
10.12016/j.issn.2096-1456.2020.01.003 |
| Popis: |
Objective To investigate the role of the bone morphogenetic protein 2 (BMP2)-Smad1/5 and p38MAPK signaling pathways in the osteogenic differentiation of MSMSCs by insulin-like growth factor 1 (IGF1).Methods A recombinant adenovirus (RAD) and IGF1 expressing IGF1 gene were constructed. After osteogenic induction, qRT-PCR and Western blot were used to detect the phosphorylation level of Smad1/5 and the expression of the BMP-2 protein in the BMP-Smad signaling pathway; immunohistochemistry was used to observe the nuclear translocation of Smad1/5; qRT-PCR and Western blot were used to detect IGF with Noggin and SB203580, inhibitors of the p38MAPK signaling pathway 1-mediated osteogenic differentiation of MSMSCs.Results The recombinant IGF1 adenovirus was constructed successfully. MSMSCs were cultured in inductive medium after infection with different concentrations of Ad-IGF1, and then, the protein levels of BMP2 and p-Smad1/5 increased. IGF1 can also induce nuclear translocation of Smad1/5. In addition, Noggin significantly reduced the phosphorylation level of Smad1/5 and the formation of mineralized nodules in the MSMSCs. The mRNA levels of Runx2, OPN and ALP also decreased. In contrast, SB203580 decreased neither the phosphorylation level of p38 nor the mRNA expression of Runx2, OPN and ALP in the Ad-IGF1 MSMSCs.Conclusion IGF1 can promote the osteogenic differentiation of MSMSCs via the BMP2-Smad1/5 signaling pathway. In contrast, IGF1 may not promote the osteogenic differentiation of MSMSCs via the p38MAPK signaling pathway. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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