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|Title:||Collagen loss and impaired wound healing is associated with c-Myb deficiency|
|Citation:||Journal of Pathology, 2007; 211(3):351-361|
|Publisher:||John Wiley & Sons Ltd|
|Z Kopecki, MM Luchetti, DH Adams, X Strudwick, T Mantamadiotis, A Stoppacciaro, A Gabrielli, RG Ramsay, AJ Cowin|
|Abstract:||Collagen type I serves as an abundant structural and signalling component of skin. It is also an established target gene of the transcription factor, c-Myb. When c-myb-/- embryos were examined it was observed that their skin was markedly thinner than normal. Importantly, immunohistochemical investigation showed complete absence of collagen type I. Although these homozygous knock-out embryos fail to develop beyond day 15, fibroblasts established from these embryos (mouse embryonic fibroblasts [MEFs]) show defective proliferative responses. Furthermore, in vitro scratch wound assays demonstrated that these c-myb-/- MEFs also exhibit slower closure than their wild-type counterparts. Embryonic lethality has meant that examination of the role of c-Myb in adult mouse skin has not been reported to date. However, in view of the abundance of collagen type I in normal skin, its role in skin integrity and the in vitro data showing proliferative and migration defects in c-myb-/- MEFs, we investigated the consequences of heterozygous c-myb loss in adult mice on the complex process of skin repair in response to injury. Our studies clearly demonstrate that heterozygous c-myb deficiency has a functional effect on wound repair, collagen type I levels and, in response to wounding, transforming growth factor-beta1 (an important collagen stimulating factor) induction expression is aberrantly high. Manipulation of c-Myb may therefore provide new therapeutic opportunities for improving wound repair while uncontrolled expression may underpin some fibrotic disorders.|
|Rights:||Copyright © 2007 Pathological Society of Great Britain and Ireland.|
|Appears in Collections:||Aurora harvest|
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