The Experts below are selected from a list of 309 Experts worldwide ranked by ideXlab platform
Andrew W Horne - One of the best experts on this subject based on the ideXlab platform.
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the Peritoneum is both a source and target of tgf β in women with endometriosis
PLOS ONE, 2014Co-Authors: Vicky J Young, Jeremy K Brown, Philippa T K Saunders, Colin W Duncan, Andrew W HorneAbstract:Transforming growth factor-b (TGF-b) 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-b and if peritoneal TGF-b 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-b1, 2 and 3 protein concentrations were measured in the peritoneal fluid. TGF-b1 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-b expression, reception and signalling by immunohistochemistry, qRT-PCR and a TGF-b signalling PCR array. TGF-b1 was increased in the peritoneal fluid of women with endometriosis compared to those without disease (P,0.05) and peritoneal mesothelial cells secrete TGF-b1 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-b-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 TGFb1 and this is enhanced around endometriosis lesions. The expression of TGF-b-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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the role of the Peritoneum in the pathogenesis of endometriosis
Human Reproduction Update, 2013Co-Authors: Vicky J Young, Jeremy K Brown, Philippa T K Saunders, Andrew W HorneAbstract:background: Endometriosis affects 6-10% of women of reproductive age and is associated with chronic pelvic pain, dysmenorrhoea, dys- pareunia and infertility. Endometriosis is defined by the presence of endometrial tissue outside the uterus, most commonly attached to the pelvic Peritoneum. The endometrium in women with endometriosis is reported to be altered and there is increasing evidence that the phenotype of the pelvic Peritoneum may also play a role in the establishment and maintenance of the disease. The aim of this review is to discuss the putative role of the pelvic Peritoneum in the pathophysiology of peritoneal endometriosis. methods: A review was undertaken of the published literature on (i) the anatomy and physiology of the Peritoneum and (ii) the potential roles played by peritoneal cells in the establishment and maintenance of peritoneal endometriosis. The current understanding of the biology of peritoneal endometriosis is summarized and the potential interaction of the Peritoneum with ectopic endometrial cells in endometriosis is highlighted. results: Several studies indicate that differential expression of peritoneal mesothelial adhesion factors occurs in women with endometriosis, providing potential ectopic endometrial cell attachment sites for the establishment of endometriosis lesions. Changes in the peritoneal mesothelial cell phenotype, including loss of tight junctions, may allow ectopic cells to bind to, or early lesions to invade into, the extracellular matrix. Epithelial- to-mesenchymal transition of peritoneal mesothelial cells may also lead to an increase in lesion invasion and formation of fibrotic tissue in and around the lesion. There is evidence that the peritoneal mesothelium may also play a role in the invasion potential of ectopic cells by production of MMPs increasing local tissue remodelling. Peritoneal immune scavenging function may be lowered in women with endometriosis; for example there is a notable increase in macrophage-derived secretion products in women with endometriosis associated with increases in cell proliferation, cell adhesion and neovascularization. conclusions: The pelvic Peritoneum appears to play a key role in the development and maintenance of endometriosis.
Vicky J Young - One of the best experts on this subject based on the ideXlab platform.
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the Peritoneum is both a source and target of tgf β in women with endometriosis
PLOS ONE, 2014Co-Authors: Vicky J Young, Jeremy K Brown, Philippa T K Saunders, Colin W Duncan, Andrew W HorneAbstract:Transforming growth factor-b (TGF-b) 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-b and if peritoneal TGF-b 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-b1, 2 and 3 protein concentrations were measured in the peritoneal fluid. TGF-b1 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-b expression, reception and signalling by immunohistochemistry, qRT-PCR and a TGF-b signalling PCR array. TGF-b1 was increased in the peritoneal fluid of women with endometriosis compared to those without disease (P,0.05) and peritoneal mesothelial cells secrete TGF-b1 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-b-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 TGFb1 and this is enhanced around endometriosis lesions. The expression of TGF-b-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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the role of the Peritoneum in the pathogenesis of endometriosis
Human Reproduction Update, 2013Co-Authors: Vicky J Young, Jeremy K Brown, Philippa T K Saunders, Andrew W HorneAbstract:background: Endometriosis affects 6-10% of women of reproductive age and is associated with chronic pelvic pain, dysmenorrhoea, dys- pareunia and infertility. Endometriosis is defined by the presence of endometrial tissue outside the uterus, most commonly attached to the pelvic Peritoneum. The endometrium in women with endometriosis is reported to be altered and there is increasing evidence that the phenotype of the pelvic Peritoneum may also play a role in the establishment and maintenance of the disease. The aim of this review is to discuss the putative role of the pelvic Peritoneum in the pathophysiology of peritoneal endometriosis. methods: A review was undertaken of the published literature on (i) the anatomy and physiology of the Peritoneum and (ii) the potential roles played by peritoneal cells in the establishment and maintenance of peritoneal endometriosis. The current understanding of the biology of peritoneal endometriosis is summarized and the potential interaction of the Peritoneum with ectopic endometrial cells in endometriosis is highlighted. results: Several studies indicate that differential expression of peritoneal mesothelial adhesion factors occurs in women with endometriosis, providing potential ectopic endometrial cell attachment sites for the establishment of endometriosis lesions. Changes in the peritoneal mesothelial cell phenotype, including loss of tight junctions, may allow ectopic cells to bind to, or early lesions to invade into, the extracellular matrix. Epithelial- to-mesenchymal transition of peritoneal mesothelial cells may also lead to an increase in lesion invasion and formation of fibrotic tissue in and around the lesion. There is evidence that the peritoneal mesothelium may also play a role in the invasion potential of ectopic cells by production of MMPs increasing local tissue remodelling. Peritoneal immune scavenging function may be lowered in women with endometriosis; for example there is a notable increase in macrophage-derived secretion products in women with endometriosis associated with increases in cell proliferation, cell adhesion and neovascularization. conclusions: The pelvic Peritoneum appears to play a key role in the development and maintenance of endometriosis.
Michael P. Diamond - One of the best experts on this subject based on the ideXlab platform.
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Expression pattern and regulation of genes differ between fibroblasts of adhesion and normal human Peritoneum
Reproductive Biology and Endocrinology, 2005Co-Authors: Ujjwal K Rout, Ghassan M. Saed, Michael P. DiamondAbstract:Background Injury to the Peritoneum during surgery is followed by a healing process that frequently results in the attachment of adjacent organs by a fibrous mass, referred commonly as adhesions. Because injuries to the Peritoneum during surgery are inevitable, it is imperative that we understand the mechanisms of adhesion formation to prevent its occurrence. This requires thorough understanding of the molecular sequence that results in the attachment of injured Peritoneum and the development of fibrous tissue. Recent data show that fibroblasts from the injured Peritoneum may play a critical role in the formation of adhesion tissues. Therefore, identifying changes in gene expression pattern in the peritoneal fibroblasts during the process may provide clues to the mechanisms by which adhesion develop. Methods In this study, we compared expression patterns of larger number of genes in the fibroblasts isolated from adhesion and normal human Peritoneum using gene filters. Contributions of TGF-beta1 and hypoxia in the altered expression of specific genes were also examined using a semiquantitative RT-PCR technique. Results Results show that several genes are differentially expressed between fibroblasts of normal and adhesion Peritoneum and that the peritoneal fibroblast may acquire a different phenotype during adhesion formation. Genes that are differentially expressed between normal and adhesion fibroblasts encode molecules involved in cell adhesion, proliferation, differentiation, migration and factors regulating cytokines, transcription, translation and protein/vesicle trafficking. Conclusions Our data substantiate that adhesion formation is a multigenic phenomenon and not all changes in gene expression pattern between normal and adhesion fibroblasts are the function of TGF-beta1 and hypoxia that are known to influence adhesion formation. Analysis of the gene expression data in the perspective of known functions of genes connote to additional targets that may be manipulated to inhibit adhesion development.
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expression pattern and regulation of genes differ between fibroblasts of adhesion and normal human Peritoneum
Reproductive Biology and Endocrinology, 2005Co-Authors: Ujjwal K Rout, Ghassan M. Saed, Michael P. DiamondAbstract:Background Injury to the Peritoneum during surgery is followed by a healing process that frequently results in the attachment of adjacent organs by a fibrous mass, referred commonly as adhesions. Because injuries to the Peritoneum during surgery are inevitable, it is imperative that we understand the mechanisms of adhesion formation to prevent its occurrence. This requires thorough understanding of the molecular sequence that results in the attachment of injured Peritoneum and the development of fibrous tissue. Recent data show that fibroblasts from the injured Peritoneum may play a critical role in the formation of adhesion tissues. Therefore, identifying changes in gene expression pattern in the peritoneal fibroblasts during the process may provide clues to the mechanisms by which adhesion develop.
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Expression of transforming growth factor beta isoform mRNA in injured Peritoneum that healed with adhesions and without adhesions and in uninjured Peritoneum
Fertility and Sterility, 2003Co-Authors: Ml Freeman, Ghassan M. Saed, Eslam El-hammady, Michael P. DiamondAbstract:Abstract Objective To compare the mRNA levels of transforming growth factor beta (TGF-β) isoforms 1, 2, and 3 among surgically injured Peritoneum that healed with adhesions, surgically injured Peritoneum that healed without adhesions, and uninjured Peritoneum. Design Prospective experimental study. Setting University vivarium. Animal(s) Fourteen sexually mature female Sprague-Dawley rats, 226–250 grams. Interventions(s) Standardized cecal abrasion was performed on 120 Sprague-Dawley rats. The areas of abrasion and any resultant adhesions were harvested at necropsy 7 days later. Total RNA was then extracted from the serosal adhesions of four rats, from the serosa of five rats that healed without adhesion formation, and from analogous areas of cecum from five rats that did not undergo abrasion and served as controls. Main outcome measure(s) Quantification of the expression of the TGF-β1, TGF-β2, and TGF-β3 mRNA transcripts in peritoneal adhesions, normally healed Peritoneum, and fresh, uninjured peritoneal tissue through the use of multiplex reverse transcriptase–polymerase chain reaction analysis. Results(s) Peritoneal adhesion TGF-β1 and TGF-β3 mRNA expression was 3.7-fold and 8.6-fold higher, respectively, than in abraded tissues that healed normally; and 5.6-fold and 4.6-fold higher, respectively, than in nonabraded tissues. While TGF-β2 mRNA levels were also higher in serosal adhesions compared with normally healed and uninjured Peritoneum, this rise was not statically significant. Conclusion(s) Peritoneal adhesions resulting from surgical abrasion of a serosal surface have statistically significant increased levels of TGF-β1 and -β3 mRNA transcripts compared with both uninjured and normally healed Peritoneum.
Jeremy K Brown - One of the best experts on this subject based on the ideXlab platform.
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the Peritoneum is both a source and target of tgf β in women with endometriosis
PLOS ONE, 2014Co-Authors: Vicky J Young, Jeremy K Brown, Philippa T K Saunders, Colin W Duncan, Andrew W HorneAbstract:Transforming growth factor-b (TGF-b) 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-b and if peritoneal TGF-b 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-b1, 2 and 3 protein concentrations were measured in the peritoneal fluid. TGF-b1 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-b expression, reception and signalling by immunohistochemistry, qRT-PCR and a TGF-b signalling PCR array. TGF-b1 was increased in the peritoneal fluid of women with endometriosis compared to those without disease (P,0.05) and peritoneal mesothelial cells secrete TGF-b1 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-b-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 TGFb1 and this is enhanced around endometriosis lesions. The expression of TGF-b-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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the role of the Peritoneum in the pathogenesis of endometriosis
Human Reproduction Update, 2013Co-Authors: Vicky J Young, Jeremy K Brown, Philippa T K Saunders, Andrew W HorneAbstract:background: Endometriosis affects 6-10% of women of reproductive age and is associated with chronic pelvic pain, dysmenorrhoea, dys- pareunia and infertility. Endometriosis is defined by the presence of endometrial tissue outside the uterus, most commonly attached to the pelvic Peritoneum. The endometrium in women with endometriosis is reported to be altered and there is increasing evidence that the phenotype of the pelvic Peritoneum may also play a role in the establishment and maintenance of the disease. The aim of this review is to discuss the putative role of the pelvic Peritoneum in the pathophysiology of peritoneal endometriosis. methods: A review was undertaken of the published literature on (i) the anatomy and physiology of the Peritoneum and (ii) the potential roles played by peritoneal cells in the establishment and maintenance of peritoneal endometriosis. The current understanding of the biology of peritoneal endometriosis is summarized and the potential interaction of the Peritoneum with ectopic endometrial cells in endometriosis is highlighted. results: Several studies indicate that differential expression of peritoneal mesothelial adhesion factors occurs in women with endometriosis, providing potential ectopic endometrial cell attachment sites for the establishment of endometriosis lesions. Changes in the peritoneal mesothelial cell phenotype, including loss of tight junctions, may allow ectopic cells to bind to, or early lesions to invade into, the extracellular matrix. Epithelial- to-mesenchymal transition of peritoneal mesothelial cells may also lead to an increase in lesion invasion and formation of fibrotic tissue in and around the lesion. There is evidence that the peritoneal mesothelium may also play a role in the invasion potential of ectopic cells by production of MMPs increasing local tissue remodelling. Peritoneal immune scavenging function may be lowered in women with endometriosis; for example there is a notable increase in macrophage-derived secretion products in women with endometriosis associated with increases in cell proliferation, cell adhesion and neovascularization. conclusions: The pelvic Peritoneum appears to play a key role in the development and maintenance of endometriosis.
Philippa T K Saunders - One of the best experts on this subject based on the ideXlab platform.
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the Peritoneum is both a source and target of tgf β in women with endometriosis
PLOS ONE, 2014Co-Authors: Vicky J Young, Jeremy K Brown, Philippa T K Saunders, Colin W Duncan, Andrew W HorneAbstract:Transforming growth factor-b (TGF-b) 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-b and if peritoneal TGF-b 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-b1, 2 and 3 protein concentrations were measured in the peritoneal fluid. TGF-b1 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-b expression, reception and signalling by immunohistochemistry, qRT-PCR and a TGF-b signalling PCR array. TGF-b1 was increased in the peritoneal fluid of women with endometriosis compared to those without disease (P,0.05) and peritoneal mesothelial cells secrete TGF-b1 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-b-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 TGFb1 and this is enhanced around endometriosis lesions. The expression of TGF-b-regulated genes is altered in the Peritoneum of women with endometriosis and this may promote an environment favorable to lesion formation.
-
the role of the Peritoneum in the pathogenesis of endometriosis
Human Reproduction Update, 2013Co-Authors: Vicky J Young, Jeremy K Brown, Philippa T K Saunders, Andrew W HorneAbstract:background: Endometriosis affects 6-10% of women of reproductive age and is associated with chronic pelvic pain, dysmenorrhoea, dys- pareunia and infertility. Endometriosis is defined by the presence of endometrial tissue outside the uterus, most commonly attached to the pelvic Peritoneum. The endometrium in women with endometriosis is reported to be altered and there is increasing evidence that the phenotype of the pelvic Peritoneum may also play a role in the establishment and maintenance of the disease. The aim of this review is to discuss the putative role of the pelvic Peritoneum in the pathophysiology of peritoneal endometriosis. methods: A review was undertaken of the published literature on (i) the anatomy and physiology of the Peritoneum and (ii) the potential roles played by peritoneal cells in the establishment and maintenance of peritoneal endometriosis. The current understanding of the biology of peritoneal endometriosis is summarized and the potential interaction of the Peritoneum with ectopic endometrial cells in endometriosis is highlighted. results: Several studies indicate that differential expression of peritoneal mesothelial adhesion factors occurs in women with endometriosis, providing potential ectopic endometrial cell attachment sites for the establishment of endometriosis lesions. Changes in the peritoneal mesothelial cell phenotype, including loss of tight junctions, may allow ectopic cells to bind to, or early lesions to invade into, the extracellular matrix. Epithelial- to-mesenchymal transition of peritoneal mesothelial cells may also lead to an increase in lesion invasion and formation of fibrotic tissue in and around the lesion. There is evidence that the peritoneal mesothelium may also play a role in the invasion potential of ectopic cells by production of MMPs increasing local tissue remodelling. Peritoneal immune scavenging function may be lowered in women with endometriosis; for example there is a notable increase in macrophage-derived secretion products in women with endometriosis associated with increases in cell proliferation, cell adhesion and neovascularization. conclusions: The pelvic Peritoneum appears to play a key role in the development and maintenance of endometriosis.