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Hepatocyte growth factor reduces CXCL 10 expression in keratinocytes
Author(s) -
Hisadome Mitsuhiro,
Ohnishi Tomokazu,
Kakimoto Kyoko,
Kusuyama Joji,
Bandow Kenjiro,
Kanekura Takuro,
Matsuguchi Tetsuya
Publication year - 2016
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12452
Subject(s) - hacat , hepatocyte growth factor , chemokine , keratinocyte , angiogenesis , vascular endothelial growth factor , microbiology and biotechnology , keratinocyte growth factor , growth factor , vascular endothelial growth factor a , biology , cancer research , mapk/erk pathway , cell culture , immunology , chemistry , inflammation , signal transduction , vegf receptors , receptor , biochemistry , genetics
Keratinocytes secrete vascular endothelial growth factor ( VEGF ) and angioregulatory chemokines during cutaneous wound healing. Hepatocyte growth factor ( HGF ) promotes skin re‐epithelialization by increasing VEGF expression in keratinocytes. Here, we investigated the regulatory roles of HGF in the expression of genes encoding angiogenic and angiostatic chemokines in keratinocytes and found that HGF specifically inhibits mRNA expression of the angiostatic chemokine CXCL 10 in both mouse primary keratinocytes and in the human keratinocyte cell line HaCaT through the MEK / ERK cascade. Furthermore, HGF inhibited tumor necrosis factor‐α‐induced CXCL 10 expression at both mRNA and protein levels in HaCaT cells. Thus, HGF may orchestrate angiogenesis in wounded skin by modulating both VEGF and CXCL 10 expression in keratinocytes.