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Stratifin as a Mediator of Epithelial/Mesenchymal Cross Talking in Skin;
Author(s) -
Ghahary Aziz
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.87.3
Subject(s) - wound healing , extracellular matrix , microbiology and biotechnology , keratinocyte , fibroblast , type i collagen , keratinocyte growth factor , skin repair , mediator , matrix (chemical analysis) , mesenchymal stem cell , chemistry , pathology , medicine , biology , immunology , cell culture , growth factor , receptor , genetics , chromatography
It is well established that any delays in epithelialization during the process of wound healing, due to either infection or severity of injury, increases the frequency of developing fibrotic conditions. This signifies that in the absence of epithelialization, the ECM continues to accumulate until fibroblasts receive signal(s) from epidermal cells to slow down the dynamic process of healing that leads to maturation and remodelling of the healing wound. Here, we provide a compelling evidence that: 1) there exist a cross‐talking between epithelial and fibroblasts using a co‐culture system, 2) Keratinocytes release two sets of ECM modulating factors that are important in controlling the healing process, 3) One set of this factors, namely stratifin, increases the expression of MMP‐1, 3, 8 and 24 in fibroblasts, 4) the other set reduces the expression of type I and type III collagen in fibroblasts, 5) On the hand, fibroblasts release some unknown factors that control the expression of keratinocyte derived anti‐fibrogenic factors (KDAF). Finally the mechanism by which these factors are released from keratinocytes will also be discussed. In conclusion, Keratinocyte releasable factors upon epithelialization may function as stop signals for matrix production by fibroblasts and that would slow down the dynamic process of healing wound.