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Lipopolysaccharides can protect mesenchymal stem cells (MSCs) from oxidative stress‐induced apoptosis and enhance proliferation of MSCs via Toll‐like receptor(TLR)‐4 and PI3K/Akt
Author(s) -
Wang Zhaojun,
Zhang Fumin,
Wang Liansheng,
Yao Yongwei,
Zhao Qiang,
Gao Xiang
Publication year - 2009
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2009.03.006
Subject(s) - mesenchymal stem cell , protein kinase b , tlr4 , pi3k/akt/mtor pathway , toll like receptor , apoptosis , chemistry , oxidative stress , microbiology and biotechnology , cancer research , receptor , signal transduction , biology , biochemistry , innate immune system
Apoptosis of implanted mesenchymal stem cells (MSCs) limits the efficiency of MSC therapy. Recent studies showed the ligands of Toll‐like receptors (TLRs) could control the function of these cells. We have investigated the effect of lipopolysaccharides (LPS), a ligand of TLR4, on the survival of MSCs and explored the roles of TLR4 and PI3K/Akt. H 2 O 2 /serum deprivation(H 2 O 2 /SD) induced apoptosis of MSCs but LPS‐preconditioning (1.0 μg/ml) protected MSCs from H 2 O 2 /SD‐induced apoptosis and promoted their proliferation. Western blotting showed that 1.0 μg/ml LPS enhanced phosphorylation of both Akt at Ser 473 and nuclear factor‐kappa B (NF‐κB) p65 at Ser 536. However, the protective effects of LPS on survival were not observed in TLR4 lps‐del MSCs. The results suggest appropriate treatments with LPS can protect MSCs from oxidative stress‐induced apoptosis and improve the survival of MSCs via the TLR4 and PI3K/Akt pathway.