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Fetuin‐A promotes primary keratinocyte migration: independent of epidermal growth factor receptor signalling
Author(s) -
Wang XueQing,
Hung Betsy S.,
Kempf Margit,
Liu PeiYun,
Dalley Andrew J.,
Saunders Nicholas A.,
Kimble Roy M.
Publication year - 2010
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2009.00978.x
Subject(s) - foreskin , keratinocyte , hacat , fetuin , dermis , microbiology and biotechnology , biology , receptor , immunology , endocrinology , medicine , chemistry , cell culture , anatomy , biochemistry , genetics , glycoprotein
Please cite this paper as : Fetuin‐A promotes primary keratinocyte migration: independent of epidermal growth factor receptor signalling. Experimental Dermatology 2010; 19 : e289–e292. Abstract: Previously, we reported that fetuin‐A is a major component of ovine foetal skin and significantly enhances ‘wound closure’ in primary keratinocyte cultures. In this study, we found that in human newborn foreskin, a high level of fetuin‐A protein is detected throughout the dermis. However, in adult skin a low level of fetuin‐A is observed throughout the epidermal and dermal layers, except at regions surrounding hair follicles and at the epidermal‐dermal junction where the level of fetuin‐A is relatively high. Fetuin‐A significantly induces actin‐rich protrusions in human primary keratinocytes. Interestingly, blockade of epidermal growth factor (EGF) receptor signalling has a limited effect on fetuin‐A promoted ‘wound closure’ on primary human keratinocytes, but significantly inhibits fetuin‐A’s effect on HaCaT cells. These results indicate that high levels of fetuin‐A may partially contribute to less scar formation in newborn foreskin and that the effect of fetuin‐A on primary keratinocyte migration is independent of EGF receptor signalling.