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A role for the collagen I/III and MMP-1/-13 genes in primary inguinal hernia?
BACKGROUND: Abnormal collagen metabolism is thought to play an important role in the development of primary inguinal hernia. This is underlined by detection of altered collagen metabolism and structural changes of the tissue in patients with primary inguinal hernia. However, it is still unknown whet...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2002
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC65699/ https://www.ncbi.nlm.nih.gov/pubmed/11872152 http://dx.doi.org/10.1186/1471-2350-3-2 |
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author | Rosch, Raphael Klinge, Uwe Si, Zhongyi Junge, Karsten Klosterhalfen, Bernd Schumpelick, Volker |
author_facet | Rosch, Raphael Klinge, Uwe Si, Zhongyi Junge, Karsten Klosterhalfen, Bernd Schumpelick, Volker |
author_sort | Rosch, Raphael |
collection | PubMed |
description | BACKGROUND: Abnormal collagen metabolism is thought to play an important role in the development of primary inguinal hernia. This is underlined by detection of altered collagen metabolism and structural changes of the tissue in patients with primary inguinal hernia. However, it is still unknown whether these alterations reflect a basic dysfunction of the collagen synthesis, or of collagen degradation. METHODS: In the present study, we analysed type I and type III procollagen messenger ribonucleic acid (mRNA) and MMP-1 and MMP-13 mRNA in cultured fibroblasts from the skin of patients with primary inguinal hernia, and from patients without hernia (controls) by reverse transcription polymerase chain reaction (RT-PCR) and Northern Blot. RESULTS: The results indicated that the ratio of type I to type III procollagen mRNA was decreased in patients with primary hernia, showing significant differences as compared to controls (p = 0.01). This decrease was mainly due to the increase of type III procollagen mRNA. Furthermore, RT-PCR analysis revealed that the expression of MMP-1 mRNA in patients with primary hernia is equivalent to that of controls (p > 0.05). In addition, MMP-13 mRNA is expressed neither in patients with primary hernia nor in controls. CONCLUSION: We concluded that abnormal change of type I and type III collagen mRNAs contribute to the development of primary inguinal hernia, whereas the expressions of MMP-1 and MMP-13 mRNA appears not to be involved in the development of primary inguinal hernia. Thus, the knowledge on the transcriptional regulation of collagen in patients with primary inguinal hernia may help to understand the pathogenesis of primary inguinal hernia, and implies new therapeutic strategies for this disease. |
format | Text |
id | pubmed-65699 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2002 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-656992002-02-28 A role for the collagen I/III and MMP-1/-13 genes in primary inguinal hernia? Rosch, Raphael Klinge, Uwe Si, Zhongyi Junge, Karsten Klosterhalfen, Bernd Schumpelick, Volker BMC Med Genet Research Article BACKGROUND: Abnormal collagen metabolism is thought to play an important role in the development of primary inguinal hernia. This is underlined by detection of altered collagen metabolism and structural changes of the tissue in patients with primary inguinal hernia. However, it is still unknown whether these alterations reflect a basic dysfunction of the collagen synthesis, or of collagen degradation. METHODS: In the present study, we analysed type I and type III procollagen messenger ribonucleic acid (mRNA) and MMP-1 and MMP-13 mRNA in cultured fibroblasts from the skin of patients with primary inguinal hernia, and from patients without hernia (controls) by reverse transcription polymerase chain reaction (RT-PCR) and Northern Blot. RESULTS: The results indicated that the ratio of type I to type III procollagen mRNA was decreased in patients with primary hernia, showing significant differences as compared to controls (p = 0.01). This decrease was mainly due to the increase of type III procollagen mRNA. Furthermore, RT-PCR analysis revealed that the expression of MMP-1 mRNA in patients with primary hernia is equivalent to that of controls (p > 0.05). In addition, MMP-13 mRNA is expressed neither in patients with primary hernia nor in controls. CONCLUSION: We concluded that abnormal change of type I and type III collagen mRNAs contribute to the development of primary inguinal hernia, whereas the expressions of MMP-1 and MMP-13 mRNA appears not to be involved in the development of primary inguinal hernia. Thus, the knowledge on the transcriptional regulation of collagen in patients with primary inguinal hernia may help to understand the pathogenesis of primary inguinal hernia, and implies new therapeutic strategies for this disease. BioMed Central 2002-02-19 /pmc/articles/PMC65699/ /pubmed/11872152 http://dx.doi.org/10.1186/1471-2350-3-2 Text en Copyright © 2002 Rosch et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL. |
spellingShingle | Research Article Rosch, Raphael Klinge, Uwe Si, Zhongyi Junge, Karsten Klosterhalfen, Bernd Schumpelick, Volker A role for the collagen I/III and MMP-1/-13 genes in primary inguinal hernia? |
title | A role for the collagen I/III and MMP-1/-13 genes in primary inguinal hernia? |
title_full | A role for the collagen I/III and MMP-1/-13 genes in primary inguinal hernia? |
title_fullStr | A role for the collagen I/III and MMP-1/-13 genes in primary inguinal hernia? |
title_full_unstemmed | A role for the collagen I/III and MMP-1/-13 genes in primary inguinal hernia? |
title_short | A role for the collagen I/III and MMP-1/-13 genes in primary inguinal hernia? |
title_sort | role for the collagen i/iii and mmp-1/-13 genes in primary inguinal hernia? |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC65699/ https://www.ncbi.nlm.nih.gov/pubmed/11872152 http://dx.doi.org/10.1186/1471-2350-3-2 |
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