Hernia fibroblasts lack beta-estradiol-induced alterations of collagen gene expression.
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 beta-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 beta-estradiol, type I and type III gene transcription is not affected in fibroblasts from males or affected females. Furthermore beta-estradiol had no influence on the impaired type I to III collagen ratio in fibroblasts from recurrent hernia patients.


CONCLUSIONS
Our results suggest that beta-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 beta-estradiol induced alterations of collagen gene expression. The observation of gender specific beta-estradiol-dependent changes of collagen gene expression in vitro is of significance for future studies of cellular response.
Lynen Jansen
Petra
P
Interdisciplinary Center for Clinical Research Biomat, University Hospital Aachen, Germany. plynen@ukaachen.de
Rosch
Raphael
R
Rezvani
Melanie
M
Mertens
Peter R
PR
Junge
Karsten
K
Jansen
Marc
M
Klinge
Uwe
U
D000005:Abdomen / Q000601:surgery; D000368:Aged; D015992:Body Mass Index; D002478:Cells, Cultured / Q000187:drug effects / Q000378:metabolism; D002921:Cicatrix / Q000378:metabolism / Q000473:pathology*; D024042:Collagen Type I / Q000096:biosynthesis* / Q000235:genetics; D000090602:Collagen Type I, alpha 1 Chain; D024061:Collagen Type III / Q000096:biosynthesis* / Q000235:genetics; D004790:Enzyme Induction / Q000187:drug effects; D004958:Estradiol / Q000494:pharmacology*; D047628:Estrogen Receptor alpha / Q000096:biosynthesis / Q000235:genetics; D047629:Estrogen Receptor beta / Q000096:biosynthesis / Q000235:genetics; D005260:Female; D005347:Fibroblasts / Q000187:drug effects* / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects*; D046449:Hernia, Abdominal / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000096:biosynthesis* / Q000235:genetics; D008875:Middle Aged; D011183:Postoperative Complications / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D012008:Recurrence; D012727:Sex Characteristics; D013529:Surgical Wound Dehiscence; D014945:Wound Healing / Q000187:drug effects
C439971:COL3A1 protein, human; D024042:Collagen Type I; D000090602:Collagen Type I, alpha 1 Chain; D024061:Collagen Type III; D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D004958:Estradiol; D020778:Matrix Metalloproteinase 2