Smads, p38 and ERK1/2 are involved in BMP9-induced osteogenic differentiation of C3H10T1/2 mesenchymal stem cells

Xu, Dao Jing; Zhao, Ying; Wang, Jin; He, Juan; Weng, Ya Guang; Luo, Jin Yong

doi:10.5483/bmbrep.2012.45.4.247

Cited by 79 publications

(77 citation statements)

References 27 publications

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“…It has been demonstrated that the roles of BMP9, 8-prenylnaringenin tigogenin, and other substances can activate the p38MAPK signaling pathway and promote osteogenic differentiation of BMMSCs [2,[4][5][6]. This collectively shows that the p38MAPK signaling pathway may play an important role in the osteogenic differentiation of BMMSCs.…”

Section: Discussionmentioning

confidence: 75%

“…Osterix knockout mice eventually succumb due to breathing difficulties and histological results have shown that there is no mineralization reaction in mice embryos. Neither endochondral ossification nor membrane ossification was completed [28][29][30]. ALP, OCN, and COL I are typically used in identification of osteogenic differentiation in cells [31].…”

Section: Discussionmentioning

confidence: 99%

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Intermittent Stretching and Osteogenic Differentiation of Bone Marrow Derived Mesenchymal Stem Cells via the p38MAPK-Osterix Signaling Pathway

Xiao

Zhang

Fan

et al. 2015

Cell Physiol Biochem

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Aims: The relationship between the p38MAPK signaling pathway and osterix in osteogenic differentiation of BMMSCs subjected to intermittent stretching was investigated. Methods: BMMSCs derived from C57BL/6J mice were divided into the following groups: 1) control, 2) stretch, and 3) SB203580+stretch (SB203580 is a p38MAPK signal pathway inhibitor). BMMSCs were exposed to an intermittent mechanical strain of 0.8% (8000μ strain) at 0.5 Hz, twice a day for 30 min each application. BMMSCs were harvested on days 1, 3, and 5 post-treatment. The expression of ALP, COL I, OCN, and osterix mRNA was assessed utilizing RT-PCR while the expression of P-p38MAPK and osterix protein was assessed by Western blot analysis. The osterix gene in mouse BMMSCs was knocked down using RNAi technology and its protein expression was also assessed by Western blot. RT-PCR was used to detect ALP, COL I, and OCN mRNA expression. Results: Intermittent stretching was found to promote expression of ALP, COL I, OCN, and osterix mRNA. Silencing the osterix gene was found to reduce levels of ALP, COL I, and OCN mRNA. Western blot analysis demonstrated that the levels of osterix and P-p38MAPK proteins in the stretch group were significantly higher than in the control group (P<0.05). There was less expression of ALP, COL I, OCN, and osterix mRNA in the SB203580+stretch group than in the control and stretch groups. Conclusions: Data demonstrate that intermittent stretching promotes osteogenic differentiation of BMMSCs, and the p38MAPK-osterix pathway has an important role in the control of osteogenesis-related gene expression.

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Section: Discussionmentioning

confidence: 75%

Section: Discussionmentioning

confidence: 99%

Intermittent Stretching and Osteogenic Differentiation of Bone Marrow Derived Mesenchymal Stem Cells via the p38MAPK-Osterix Signaling Pathway

Xiao

Zhang

Fan

et al. 2015

Cell Physiol Biochem

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“…Activation of p38 MAPK is essential for BMP9-induced osteogenesis in mesenchymal progenitor cells (49,54,55). However, BMP9 failed to activate p38 MAPK in 143B cells (Fig.…”

Section: Discussionmentioning

confidence: 89%

All-trans retinoic acid restored the osteogenic ability of BMP9 in osteosarcoma through the p38 MAPK pathway

Meng

et al. 2017

International Journal of Oncology

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Abstract. Osteosarcoma (OS) is the most common malignant bone tumour and is considered to be a disease caused by a dysfunction in differentiation. Bone morphogenetic protein 9 (BMP9) is the most potent osteogenic factor in mesenchymal stem cells, but it cannot induce osteogenic differentiation in OS cells; this might be one of the determinants in the pathogenesis of OS. All-trans retinoic acid (ATRA) can induce osteogenic differentiation of OS cells and potentiate BMP9-induced osteogenesis in preadipocytes. However, the concomitant effect of ATRA and BMP9 in OS cells is unclear; therefore, in the present study, we focused on this topic. The results showed that BMP9 significantly promoted the proliferation of human OS 143B cells and did not induce osteogenic differentiation of cells in vitro (p<0.01). ATRA inhibited proliferation and induced osteogenesis in 143B cells; these effects could be enhanced by BMP9 overexpression (p<0.05). ATRA could significantly increase the level of phosphorylated p38 MAPK (p-p38) in 143B cells, while BMP9 did not have any significant effect. Notably, BMP9 overexpression enhanced the ability of ATRA to increase the levels of p-p38. Both the osteogenic differentiation and the anti-proliferative activity of BMP9 in the presence of ATRA decreased upon treatment with a specific inhibitor of p38 MAPK (SB203580) (p<0.01). This study indicates that the osteogenic differentiation ability of BMP9 in 143B cells can be restored by ATRA, and the combination of BMP9 and ATRA generated a stronger anti-proliferative effect on 143B cells than ATRA alone. This result may be due to the activation of the p38 MAPK pathway.

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“…In recent years, BMP9, as a new class of BMP, has been widely studied for its strong impact on the induction of MSC differentiation. However, its mechanism and correlation with traditional transforming factors remain unknown (Xu et al, 2012). In this study, we found that BMP9 mainly affects MSC differentiation through the mitogen-activated protein kinase (MAPK) pathway.…”

Section: Introductionmentioning

confidence: 81%

Synergistic effect of BMP9 and TGF-β in the proliferation and differentiation of osteoblasts

Li¹,

Liu²,

Ma³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. We investigated the synergistic effect of bone morphogenetic protein 9 (BMP9) and transforming growth factor (TGF)-b in the transformation of mesenchymal stem cells into osteoblasts. We evaluated the effect of BMP9 and TGF-b on the induction of osteoblast formation. Mitogen-activated protein kinase (MAPK) pathway-related proteins such as p38, extracellular receptor kinase 1/2, and c-Jun N-terminal kinase (JNK) were analyzed. The interactions between TGF-Smad and BMP-MAPK were also studied. BMP9 alone induced the differentiation of mesenchymal stem cells (MSCs) into osteoblasts and enhanced phosphorylation of p38, extracellular receptor kinase 1/2, and JNK. TGF-b alone failed to induce transformation, but could increase the effect of X.L. Li et al. 7606©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (3): 7605-7615 (2015) BMP9. In this process the activation of Smad resulted in activation of the JNK pathway in the MAPK pathway. BMP9 induced osteogenesis of MSC differentiation through the MAKP pathway, while TGF-b contributed to BMP9 enhancement through the Smad-JNK pathway.

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Smads, p38 and ERK1/2 are involved in BMP9-induced osteogenic differentiation of C3H10T1/2 mesenchymal stem cells

Cited by 79 publications

References 27 publications

Intermittent Stretching and Osteogenic Differentiation of Bone Marrow Derived Mesenchymal Stem Cells via the p38MAPK-Osterix Signaling Pathway

Intermittent Stretching and Osteogenic Differentiation of Bone Marrow Derived Mesenchymal Stem Cells via the p38MAPK-Osterix Signaling Pathway

All-trans retinoic acid restored the osteogenic ability of BMP9 in osteosarcoma through the p38 MAPK pathway

Synergistic effect of BMP9 and TGF-β in the proliferation and differentiation of osteoblasts

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