Intest Res.
2009 Jun;7(1):32-40.
Expression of Matrix Metallopreoteinases and Tissue Inhibitors of Metalloproteinases in Ulcerative Colitis
- Affiliations
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- 1Department of Internal Medicine, Ewha Womans University School of Medicine, Ewha Medical Research Institute, Seoul, Korea. jassa@ewha.ac.kr
Abstract
- BACKGROUND/AIMS
Ulcerative colitis (UC) is characterized by chronic non-specific inflammation in the mucosa and submucosa of the colon. Degradation of the extracellular matrix (ECM) is one of the major events during this process. Matrix metalloproteinases (MMPs) are important enzymes involved in the degradation of the ECM, and the activities of MMPs are controlled by its natural inhibitor, tissue inhibitor of metalloproteinases (TIMPs). This study was performed to determine the expression of MMPs and TIMPs in patients with UC.
METHODS
Twenty-nine patients with UC and 5 controls were included. Colonoscopic biopsies were obtained from the cecum, ascending colon, transverse colon, sigmoid colon, and rectum in each patient. The mRNA levels of expression of MMP-2 and -9, and TIMP-1 and -2 were measured separately using reverse transcription polymerase chain reactions in the mucosal specimens from each 5 segments of the colon.
RESULTS
The mRNA expression of MMP-2 and -9, and TIMP-1 in the inflamed tissues of patients with UC was significantly increased compared to non-inflamed tissues of patients with UC and controls (p<0.05). The mRNA expression of MMP-9 and TIMP-1 in non-inflamed tissues of patients with UC was significantly higher than that of controls (p<0.05). In inflamed tissues of UC, the mRNA expression of MMP-2 was significantly correlated with TIMP-2, and the mRNA expression of MMP-9 was significantly correlated with TIMP-1. The MMP-2/TIMP-2 ratio was increased in inflamed tissues compared to non-inflamed tissues of patients with UC and controls (p<0.05).
CONCLUSIONS
MMP-2 and-9, and TIMP-1 are likely to contribute to the inflammatory cascade in UC. MMP-2 and-9, and TIMP-1 might be important clues to solve the pathogenesis of UC.