A role for the collagen I/III and MMP-1/-13 genes in primary inguinal hernia?

Abstract

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.

Figure 1

PCR products analysis of type I and type III collagen samples and β-actin optimisation. 1, 2 and 3) controls; 4, 5 and 6) inguinal hernias; 7) standard marker, a) β-actin amplification with annealing temperature at 60°C of type I collagen; b) β-actin amplification with annealing temperature at 44°C of type III collagen; c) type I collagen; d) type III collagen

Figure 2

Northern Blot analysis of type I and type III collagen mRNA from cultured fibroblasts. The ratio of 28S to 18S rRNA (ribosomal RNA) was approximately 2 : 1 by ethidium bromide staining of denaturing agarose gel electrophoresis, indicating that no gross degradation of extracted RNA occurred. 1. primary inguinal hernia; 2 control

Figure 3

PCR products analysis of MMP-1 samples. 1, 2 and 3) controls; 4, 5 and 6) primary hernias; 7) standard marker.