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• W2130114747 abstract "Abstract Objective The aetiology of inguinal hernia involves changes in collagen turnover and metalloproteinase expression; yet it is not known whether the elastic fibre system could also be affected. This study was designed to compare the expression of tropoelastin (TE), lysyl oxidase‐like 1 (LOXL‐1) and elastase in the transversalis fascia of patients with and without inguinal hernia. Material and methods Transversalis fascia (TF) specimens were obtained from patients undergoing surgery for direct or indirect inguinal hernia ( n = 20 each) and from multi‐organ donors during organ procurement (controls, n = 16). The specimens were divided according to age (20–40/41–60 years). Tissues were immunohistochemically labelled using anti‐tropoelastin, anti‐LOXL‐1 and anti‐elastase antibodies and subjected to Western blot analysis. Relative amounts of LOXL‐1 and TE mRNA were determined by real time RT‐PCR in cultured cells obtained from the TF of patients and controls. Results Significantly lower TE and LOXL‐1 levels were observed in patients with direct inguinal hernia compared with controls or those with indirect hernia. In contrast, patients with direct inguinal hernia showed significantly higher elastase expression. In fibroblasts isolated from the TF, relative amounts of tropoelastin mRNA were lower for the hernia groups but differences were not significant. LOXL‐1 mRNA levels were significantly lower in the direct hernia group compared to controls. Conclusions Our findings suggest that impaired elastic fibre function in the transversalis fascia of patients with direct inguinal hernia, reflected by diminished elastin synthesis and its enhanced enzyme degradation, contributes to the development of this type of hernia." @default.
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• W2130114747 date "2009-03-09" @default.
• W2130114747 modified "2023-10-15" @default.
• W2130114747 title "Lysyl oxidase like-1 dysregulation and its contribution to direct inguinal hernia" @default.
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• W2130114747 doi "https://doi.org/10.1111/j.1365-2362.2009.02099.x" @default.
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