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Procollagen type I gene expression and cell proliferation are increased in lipodermatosclerosis
Author(s) -
DeGiorgioMiller A.M.,
Treharne L.J.,
McAnulty R.J.,
Coleridge Smith P.D.,
Laurent G.J.,
Herrick S.E.
Publication year - 2005
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2004.06243.x
Subject(s) - procollagen peptidase , dermis , chronic venous insufficiency , fibrosis , medicine , biopsy , gene expression , type i collagen , hyperpigmentation , skin biopsy , pathology , cell growth , wound healing , inflammation , fibroblast , biology , immunology , cell culture , gene , dermatology , biochemistry , genetics
Summary Background Lipodermatosclerosis (LDS) is characterized by a hardening and hyperpigmentation of lower leg skin as a consequence of chronic venous insufficiency. The degree of skin hardening or fibrosis associated with LDS is proposed to relate directly to skin breakdown and venous ulcer formation as well as to a subsequent delay in ulcer healing. Objectives To determine whether elevated procollagen type I gene expression and increased cell proliferation are responsible for the fibrotic changes associated with LDS. Methods Skin biopsies were obtained from the legs of patients with varying degrees of chronic venous disease and were assessed for procollagen gene expression by in‐situ hybridization and for cell proliferation by immunolocalization of proliferating cell nuclear antigen. Results The number of cells expressing procollagen type I mRNA ( COL1A1 ) was significantly higher in the dermis of LDS‐affected skin compared with samples from the other patient groups. In addition, there was a significant increase in the number of dermal fibroblasts undergoing proliferation in both LDS samples and skin samples prior to LDS changes compared with control samples. However, there was no significant difference in level of inflammation in biopsy samples between patient classes. Conclusions These results suggest that enhanced cell proliferation and procollagen gene expression are both involved in LDS development. Furthermore, fibrotic changes may occur in the absence of, or subsequent to, any significant inflammatory response, indicating that additional profibrotic factors produced in the skin as a consequence of chronic venous insufficiency may play a role in LDS formation.