ArticleMolecular medicine reports2018
PDGF‑BB promotes the differentiation and proliferation of MC3T3‑E1 cells through the Src/JAK2 signaling pathway.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
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- Dynamic chromatin accessibility and transcriptome changes following PDGF-BB treatment of bone-marrow derived mesenchymal stem cells.BMC genomics · 2024Article
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- Platelet-derived growth factor PDGF-AA upregulates connexin 43 expression and promotes gap junction formations in osteoblast cells throughBiochemistry and biophysics reports · 2023Article
- Myositis ossificans circumscripta after surgery and radiotherapy and during sunitinib treatment: a case report.Journal of medical case reports · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Platelet‑derived growth factor‑BB (PDGF‑BB) serves a critical function in human osteoblast differentiation and proliferation. Src and Janus kinase 2 (JAK2) are involved in these processes. In our previous study, it was identified that Src could promote the phosphorylation of JAK2. However, it has yet to be determined whether the Src/JAK2 signaling pathway affects PDGF‑BB‑mediated osteoblast differentiation and proliferation. In the present study, western blotting, polymerase chain reaction, alizarin red staining, alkaline phosphatase and Cell Counting kit‑8 were employed to explore these questions. Firstly, it was demonstrated that PDGF‑BB activates the Src/JAK2 signaling pathway in MC3T3‑E1 cells in a time‑dependent manner. Furthermore, it was demonstrated that PDGF‑BB expression promoted MC3T3‑E1 cell differentiation and proliferation; this process was suppressed by AG1295, SU6656 and AG490, which are inhibitors of PDGFR‑β, Src and JAK2, respectively. SU6656 downregulated the activity of Src and JAK2, while AG490 only downregulated JAK2 activity. Therefore, it was concluded that Src is upstream of JAK2. PDGF‑BB also upregulated the expression of osteogenesis‑associated genes, and the formation of mineral nodules. However, these effects were markedly inhibited by treatment with SU6656. This indicated that PDGF‑BB promoted MC3T3‑E1 cell differentiation and proliferation by activating the Src/JAK2 signaling pathway. These results suggested that PDGF‑BB may have potential applications in the treatment of osteoporosis and bone fractures.
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