Open AccessNegative pressure wound therapy promotes muscle‐derived stem cell osteogenic differentiation through MAPK pathway
Author(s) -
Liu Hong,
Zheng Xun,
Chen Liang,
Jian Chao,
Hu Xiang,
Zhao Yong,
Li Zonghuan,
Yu Aixi
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13339
Subject(s) - runx2 , mapk/erk pathway , p38 mitogen activated protein kinases , cell growth , apoptosis , cellular differentiation , cell , chemistry , microbiology and biotechnology , cancer research , signal transduction , medicine , gene expression , biology , gene , biochemistry
Negative pressure wound therapy ( NPWT ) has been revealed to be effective in the treatment of open fractures, although the underlying mechanism is not clear. This article aimed to investigate the effects of NPWT on muscle‐derived stem cell ( MDSC ) osteoblastic differentiation and the related potential mechanism. The cell proliferation rate was substantially increased in NPWT ‐treated MDSC s in comparison with a static group for 3 days. There was no observable effect on the apoptosis of MDSC treated with NPWT compared with the control group for 3 days. The expression levels of HIF ‐1α, BMP ‐2, COL ‐I, OST and OPN were increased on days 3, 7 and 14, but the expression level of Runx2 was increased on days 3 and 7 in the NPWT group. Pre‐treatment, the specific inhibitors were added into the MDSC s treated with NPWT and the control group. ALP activity and mineralization were reduced by inhibiting the ERK 1/2, p38 and JNK pathways. The expression levels of Runx2, COL ‐I, OST and OPN genes and proteins were also decreased using the specific MAPK pathway inhibitors on days 3, 7 and 14. There were no significant effects on the expression of BMP ‐2 except on day 3. However, the expressions of the HIF ‐1α gene and protein slightly increased when the JNK pathway was inhibited. Therefore, NPWT promotes the proliferation and osteogenic differentiation of MDSC s through the MAPK pathway.