The peritoneum is both a source and target of TGF-β in women with endometriosis.

Transforming growth factor-β (TGF-β) is believed to play a major role in the aetiology of peritoneal endometriosis. We aimed to determine if the peritoneum is a source of TGF-β and if peritoneal TGF-β expression, reception or target genes are altered in women with endometriosis. Peritoneal fluid, pe...

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Main Authors: Vicky J Young, Jeremy K Brown, Philippa T K Saunders, W Colin Duncan, Andrew W Horne
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0106773
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author Vicky J Young
Jeremy K Brown
Philippa T K Saunders
W Colin Duncan
Andrew W Horne
author_facet Vicky J Young
Jeremy K Brown
Philippa T K Saunders
W Colin Duncan
Andrew W Horne
author_sort Vicky J Young
collection DOAJ
description Transforming growth factor-β (TGF-β) is believed to play a major role in the aetiology of peritoneal endometriosis. We aimed to determine if the peritoneum is a source of TGF-β and if peritoneal TGF-β expression, reception or target genes are altered in women with endometriosis. Peritoneal fluid, peritoneal bushings and peritoneal biopsies were collected from women with and without endometriosis. TGF-β1, 2 and 3 protein concentrations were measured in the peritoneal fluid. TGF-β1 was measured in mesothelial cell conditioned media. Control peritoneum and peritoneum prone to endometriosis (within Pouch of Douglas) from women without disease (n = 16) and peritoneum distal and adjacent to endometriosis lesions in women with endometriosis (n = 15) and were analysed for TGF-β expression, reception and signalling by immunohistochemistry, qRT-PCR and a TGF-β signalling PCR array. TGF-β1 was increased in the peritoneal fluid of women with endometriosis compared to those without disease (P<0.05) and peritoneal mesothelial cells secrete TGF-β1 in-vitro. In women with endometriosis, peritoneum from sites adjacent to endometriosis lesions expressed higher levels of TGFB1 mRNA when compared to distal sites (P<0.05). The TGF-β-stimulated Smad 2/3 signalling pathway was active in the peritoneum and there were significant increases (P<0.05) in expression of genes associated with tumorigenesis (MAPK8, CDC6), epithelial-mesenchymal transition (NOTCH1), angiogenesis (ID1, ID3) and neurogenesis (CREB1) in the peritoneum of women with endometriosis. In conclusion, the peritoneum, and in particular, the peritoneal mesothelium, is a source of TGF-β1 and this is enhanced around endometriosis lesions. The expression of TGF-β-regulated genes is altered in the peritoneum of women with endometriosis and this may promote an environment favorable to lesion formation.
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spelling doaj-art-196ed9fb68204d2bac0cbde5e1997c9b2025-08-20T02:22:45ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0199e10677310.1371/journal.pone.0106773The peritoneum is both a source and target of TGF-β in women with endometriosis.Vicky J YoungJeremy K BrownPhilippa T K SaundersW Colin DuncanAndrew W HorneTransforming growth factor-β (TGF-β) is believed to play a major role in the aetiology of peritoneal endometriosis. We aimed to determine if the peritoneum is a source of TGF-β and if peritoneal TGF-β expression, reception or target genes are altered in women with endometriosis. Peritoneal fluid, peritoneal bushings and peritoneal biopsies were collected from women with and without endometriosis. TGF-β1, 2 and 3 protein concentrations were measured in the peritoneal fluid. TGF-β1 was measured in mesothelial cell conditioned media. Control peritoneum and peritoneum prone to endometriosis (within Pouch of Douglas) from women without disease (n = 16) and peritoneum distal and adjacent to endometriosis lesions in women with endometriosis (n = 15) and were analysed for TGF-β expression, reception and signalling by immunohistochemistry, qRT-PCR and a TGF-β signalling PCR array. TGF-β1 was increased in the peritoneal fluid of women with endometriosis compared to those without disease (P<0.05) and peritoneal mesothelial cells secrete TGF-β1 in-vitro. In women with endometriosis, peritoneum from sites adjacent to endometriosis lesions expressed higher levels of TGFB1 mRNA when compared to distal sites (P<0.05). The TGF-β-stimulated Smad 2/3 signalling pathway was active in the peritoneum and there were significant increases (P<0.05) in expression of genes associated with tumorigenesis (MAPK8, CDC6), epithelial-mesenchymal transition (NOTCH1), angiogenesis (ID1, ID3) and neurogenesis (CREB1) in the peritoneum of women with endometriosis. In conclusion, the peritoneum, and in particular, the peritoneal mesothelium, is a source of TGF-β1 and this is enhanced around endometriosis lesions. The expression of TGF-β-regulated genes is altered in the peritoneum of women with endometriosis and this may promote an environment favorable to lesion formation.https://doi.org/10.1371/journal.pone.0106773
spellingShingle Vicky J Young
Jeremy K Brown
Philippa T K Saunders
W Colin Duncan
Andrew W Horne
The peritoneum is both a source and target of TGF-β in women with endometriosis.
PLoS ONE
title The peritoneum is both a source and target of TGF-β in women with endometriosis.
title_full The peritoneum is both a source and target of TGF-β in women with endometriosis.
title_fullStr The peritoneum is both a source and target of TGF-β in women with endometriosis.
title_full_unstemmed The peritoneum is both a source and target of TGF-β in women with endometriosis.
title_short The peritoneum is both a source and target of TGF-β in women with endometriosis.
title_sort peritoneum is both a source and target of tgf β in women with endometriosis
url https://doi.org/10.1371/journal.pone.0106773
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