Open Access Highly Accessed Research article

Hernia fibroblasts lack β-estradiol induced alterations of collagen gene expression

Petra Lynen Jansen1*, Raphael Rosch2, Melanie Rezvani2, Peter R Mertens3, Karsten Junge2, Marc Jansen2 and Uwe Klinge2

Author affiliations

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

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Citation and License

BMC Cell Biology 2006, 7:36  doi:10.1186/1471-2121-7-36

Published: 29 September 2006



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.


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.


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.