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Updated: Feb 6, 2026

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
Published on: February 21, 2018
PDGF‑BB promotes the differentiation and proliferation of MC3T3‑E1 cells through the Src/JAK2 signaling pathway
Qi Liu1, Yunfeng Zhou1, Zubing Li2
1The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei‑MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, Wuhan University, Wuhan, Hubei 430079, P.R. China.
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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