Expression pattern and regulation of genes differ between fibroblasts of adhesion and normal human peritoneum

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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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Published 01 January 2005
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Published: 10 January 2005 Received: 30 August 2004 Reproductive Biology and Endocrinology 2005, 3 :1 doi:10.1186/1477-7827-3-1 Accepted: 10 January 2005 This article is available from: http://www.rbej.com/content/3/1/1 © 2005 Rout et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons. org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the orig inal work is properly cited.
Abstract Background: Injury to the peritoneum during surger y is followed by a healing process that frequently results in the attachment of adjace nt organs by a fibrous mass, referred commonly as adhesions. Because injuries to the peritoneum during surgery are inev itable, it is imperative that we understand the mechanisms of adhesion formation to prevent its occurrence. This requires thorough understanding of the molecular sequenc e 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 hu man 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 differenti ally expressed between fibroblasts of normal and adhesion peritoneum and th at the peritoneal fibroblast may acquire a different phenotype during adhesion formation. Genes that are diff erentially expressed betw een normal and adhesion fibroblasts encode molecules involved in cell adhe sion, proliferation, differentiation, migration and factors regulating cytokines, transcription, translation an d protein/vesicle trafficking. Conclusions: Our data substantiate that adhesion form ation is a multigenic phenomenon and not all changes in gene expression pattern between no rmal and adhesion fibroblasts are the function of TGF-beta1 and hypoxia that are known to influe nce adhesion formation. Analysis of the gene expression data in the perspective of known functions of genes co nnote to additional targets that may be manipulated to inhibit adhesion development.
Background infertility [1]. Epidemiological studies conclude that 30 to Peritoneal adhesions resulting from surgical injury are 35% of all hospital readmissions are associated with often associated with pelvic pain, bowel obstruction and adhesion associated complications, of which 4.5 to 5.1%
Bio Med  Central
Address: 1 Division of Reproduction Endocrinology and Infertility, Departme nt of Obstetrics and Gynecology , Wayne State University, School of Medicine, Detroit, MI 48201, USA and 2 Division of Pediatric Surgery, Depa rtment of Surgery, University of Mississippi Medical Center, Jackson, MS 39216, USA Email: Ujjwal K Rout* - urout@s urgery.umsmed.edu; Ghassan M Saed - g.saed@wayne.edu; Mich ael P Diamond - mpdmd@aol.com * Corresponding author
Research Open Access Expression pattern and regulati on of genes differ between fibroblasts of adhesion an d normal human peritoneum Ujjwal K Rout* 1,2 , Ghassan M Saed 1 and Michael P Diamond 1