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Migration of bone marrow‐derived mesenchymal stem cells induced by tumor necrosis factor‐α and its possible role in wound healing
Author(s) -
Fu Xiaobing,
Han Bing,
Cai Sa,
Lei Yonghong,
Sun Tongzhu,
Sheng Zhiyong
Publication year - 2009
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1111/j.1524-475x.2009.00454.x
Subject(s) - mesenchymal stem cell , tumor necrosis factor alpha , mapk/erk pathway , microbiology and biotechnology , p38 mitogen activated protein kinases , signal transduction , cancer research , kinase , blot , chemistry , wound healing , chemotaxis , biology , immunology , receptor , biochemistry , gene
We aimed to investigate the effect of tumor necrosis factor‐α (TNF‐α) on the expression of intercellular adhesion molecule‐1 (ICAM‐1) and vascular cell adhesion molecule‐1 (VCAM‐1) in the migration ability of mesenchymal stem cells (MSCs) in the context of wound healing. We also explored the role of p38 mitogen‐activated protein kinase and extracellular signal‐regulated kinase (ERK) signaling pathways in the migration of MSCs. MSCs were isolated from the bone marrow and cultured. Immunocytochemistry, Western blotting, and reverse transcription‐polymerase chain reaction were used to observe the effect of TNF‐α on the expression of ICAM‐1 and VCAM‐1 in MSCs. The chemotaxis effect of TNF‐α on MSCs was investigated by the trans‐well system and the inhibition effect of TNF‐α using its antibody. Western blotting analysis was used to observe the activation of JAK‐STAT and mitogen‐activated protein kinase signaling pathways, and ERK was inhibited with PD98059 and p38 with SB203580 to observe the effect of TNF‐α on MSC migration and ICAM‐1 expression. The expression of ICAM‐1 could be up‐regulated by 50 μg/L TNF‐α ( p <0.05), whereas that of VCAM‐1 remained unchanged ( p >0.05). Also, TNF‐α showed a chemotaxis effect by enhancing the migration ability of MSCs ( p <0.05). TNF‐α at 50 μg/L increased the expression of phospho‐ERK and phospho‐p38, and SB203580, but not PD98059, could suppress the chemotaxis effect and up‐regulation of ICAM‐1 induced by TNF‐α in MSCs ( p <0.05). Thus, TNF‐α could up‐regulate the expression of ICAM‐1 in MSCs and enhance the cells' migration ability, and the p38 signaling pathway might be involved in the TNF‐α–induced migration ability for a role in wound repair and regeneration.