BMC Cell Biology
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 Research articleHernia fibroblasts lack β-estradiol induced alterations of collagen gene expressionPetra Lynen Jansen1 , Raphael Rosch2 , Melanie Rezvani2 , Peter R Mertens3 , Karsten Junge2 , Marc Jansen2 and Uwe Klinge2  1
Interdisciplinary Center for Clinical Research Biomat, University Hospital Aachen, Germany 2
Department of Surgery, University Hospital Aachen, Germany 3
Department of Nephrology and Clinical Immunology, University Hospital Aachen, Germany author email corresponding author email
BMC Cell Biology 2006,
7:36doi:10.1186/1471-2121-7-36
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29 September 2006 |
Abstract
Background
Estrogens are reported to increase type I and type III collagen deposition and to regulate Metalloproteinase 2 (MMP-2) expression. These proteins are reported to be dysregulated in incisional hernia formation resulting in a significantly decreased type I to III ratio. We aimed to evaluate the β-estradiol mediated regulation of type I and type III collagen genes as well as MMP-2 gene expression in fibroblasts derived from patients with or without history of recurrent incisional hernia disease. We compared primary fibroblast cultures from male/female subjects without/without incisional hernia disease.
Results
Incisional hernia fibroblasts (IHFs) revealed a decreased type I/III collagen mRNA ratio. Whereas fibroblasts from healthy female donors responded to β-estradiol, type I and type III gene transcription is not affected in fibroblasts from males or affected females. Furthermore β-estradiol had no influence on the impaired type I to III collagen ratio in fibroblasts from recurrent hernia patients.
Conclusion
Our results suggest that β-estradiol does not restore the imbaired balance of type I/III collagen in incisional hernia fibroblasts. Furthermore, the individual was identified as an independent factor for the β-estradiol induced alterations of collagen gene expression. The observation of gender specific β-estradiol-dependent changes of collagen gene expression in vitro is of significance for future studies of cellular response. |