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Crosstalk of EGF‐directed MAPK signalling pathways and its potential role on EGF‐induced cell proliferation and COX‐2 expression in human mesenchymal stem cells
Author(s) -
Sabri Abdullah,
Ziaee AbedAli,
Ostad Seyed Nasser,
Alimoghadam Kamran,
Ghahremani Mohammad Hossein
Publication year - 2011
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1720
Subject(s) - epidermal growth factor , microbiology and biotechnology , pi3k/akt/mtor pathway , protein kinase b , mesenchymal stem cell , cell growth , mapk/erk pathway , signal transduction , crosstalk , p38 mitogen activated protein kinases , chemistry , biology , cancer research , cell culture , biochemistry , genetics , physics , optics
Epidermal growth factor (EGF) promotes proliferation in human mesenchymal stem cells (hMSCs) during in vitro propagation. In this study, we investigated the effects of PI3K/AKT, ERK1/2, P38 and JNK on EGF signalling in hMSCs. The effects of EGF on MAPKs and PI3K/AKT crosstalk were investigated by immunoblotting; cyclooxygenase‐2 (COX‐2) expression was studied by real‐time RT‐PCR; and cell proliferation was evaluated by methylthiazolyl tetrazolium bromide assay. Our results showed that EGF immediately activated all four pathways, induced proliferation and increased COX‐2 expression. Interestingly, inhibition of PI3K/AKT‐enhanced EGF‐stimulated ERK1/2 activity, and inhibition of ERK1/2 and JNK reduced AKT phosphorylation. Furthermore, EGF‐induced proliferation as well as EGF‐augmented COX2 expression was hindered by ERK1/2 and p38 inhibitors. The results of this study provide evidences to be used in extended proliferation of hMSCs for cell therapy. Copyright © 2011 John Wiley & Sons, Ltd.