Analysis of collagen-interacting proteins in patients with incisional hernias
- 15 January 2003
- journal article
- research article
- Published by Springer Nature in Langenbecks Archives Of Surgery
- Vol. 387 (11-12) , 427-432
- https://doi.org/10.1007/s00423-002-0345-3
Abstract
Background In recent years a disorder of the collagen metabolism has been suggested for the pathogenesis of abdominal wall hernias. Previous investigations of skin specimens revealed a reduction in the collagen I/III ratio and alterations in matrix metalloproteinases in patients with incisional hernias. We investigated known collagen-interacting proteins to further characterize connective tissue in these patients. Patients and methods Skin scars from patients with either primary or recurrent incisional and recurrent inguinal hernias, as a subgroup of incisional hernias, were analyzed for overall collagen content and for the distribution of collagen types I and III by crosspolarization microscopy. The expression of collagen type V, collagen receptor discoidin domain receptor 2, matrix metalloproteinase 1, connective tissue-like growth factor, and tenascin was determined by immunohistochemistry. Mature abdominal skin scars from patients without evident hernia served as controls. Results Patients with recurrent incisional hernia showed lowest ratios of collagen types I to III. Contents of overall collagen and of collagen type V did not differ between the groups. In patients with either primary or recurrent incisional hernias the proportion of collagen receptor discoidin domain receptor 2 positive cells was increased. Matrix metalloproteinase 1 expression was more pronounced in patients with recurrent incisional or inguinal hernias than in controls. Connective tissue-like growth factor was significantly increased in recurrent inguinal hernia patients. The expression of tenascin was notably decreased in all hernia groups. Conclusions The observed alterations in the expression of collagen-interacting proteins again indicate the possibility of a fundamental connective tissue disease as the causal factor in the pathogenesis of (recurrent) incisional hernias.Keywords
This publication has 38 references indexed in Scilit:
- Expression of Type I Procollagen GenesPublished by Wiley ,2007
- Null Alleles of the COL5A1 Gene of Type V Collagen Are a Cause of the Classical Forms of Ehlers-Danlos Syndrome (Types I and II)American Journal of Human Genetics, 2000
- COL5A1 Haploinsufficiency Is a Common Molecular Mechanism Underlying the Classical Form of EDSAmerican Journal of Human Genetics, 2000
- Metalloproteinase inhibitors and wound healing: A novel enhancer of wound strengthSurgery, 1998
- Targeted mutation in the col5a2 gene reveals a regulatory role for type V collagen during matrix assemblyNature Genetics, 1995
- Increased collagen synthesis and decreased collagen degradation in right ventricular hypertrophy induced by pressure overloadCardiovascular Research, 1994
- The clinical features of Ehlers-Danlos syndrome type VIIB resulting from a base substitution at the splice acceptor site of intron 5 of the COL1A2 gene.Journal of Medical Genetics, 1994
- Inguinal hernia in patients with congenital dislocation of the hip: A sign of general connective tissue disorderActa Orthopaedica, 1988
- Necrobiosis Lipoidica: Ultrastructural and Biochemical Demonstration of a Collagen DefectJournal of Investigative Dermatology, 1987
- Differential histologic diagnosis of osteoid. A study on human osteosarcoma collagen by the histochemical picrosirius‐polarization methodThe Journal of Pathology, 1986