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Publication Record


Lack of MMP10 exacerbates experimental colitis and promotes development of inflammation-associated colonic dysplasia.
Koller FL, Dozier EA, Nam KT, Swee M, Birkland TP, Parks WC, Fingleton B
(2012) Lab Invest 92: 1749-59
MeSH Terms: Animals, Bone Marrow, Bone Marrow Transplantation, Cell Line, Colitis, Ulcerative, Colon, Cytokines, Dextran Sulfate, Disease Models, Animal, Female, Histocytochemistry, Humans, Inflammatory Bowel Diseases, Leukocytes, Male, Matrix Metalloproteinase 10, Mice, Mice, Inbred C57BL, Mice, Knockout, Real-Time Polymerase Chain Reaction
Show Abstract · Added March 7, 2014
Inflammatory bowel diseases (IBD) such as ulcerative colitis (UC) represent serious health burdens because of both the tissue-damaging disease itself and an elevated risk of colon cancer. The increased expression of many members of the matrix metalloproteinase (MMP) family of enzymes that occurs in colitis has long been associated with the destructive nature of the disease. Recent findings in cancer and other MMP-associated diseases, however, led us to question whether MMPs are indeed detrimental in the setting of colitis. Here, we focus on a single MMP family member, MMP10, and assess its role in a murine model of colonic tissue damage induced by dextran sulfate sodium (DSS) treatment. Using mice genetically deficient for MMP10, we find that absence of this enzyme leads to significantly worse disease scores and failure to resolve inflammation even after extended recovery periods. We show that MMP10 is produced predominantly by infiltrating myeloid cells in both murine and human colitis. Through bone marrow transplant experiments, we confirm that bone marrow-derived MMP10 contributes to colitis severity. Mice lacking MMP10 have a significantly higher propensity for development of dysplastic lesions in the colon after two rounds of DSS exposure. Thus, we conclude that MMP10 is required for resolution of DSS-induced colonic damage, and in its absence, chronic inflammation and ultimately dysplasia occurs.
1 Communities
2 Members
0 Resources
20 MeSH Terms
Expression and localization of the matrix metalloproteinase pump-1 (MMP-7) in human gastric and colon carcinomas.
McDonnell S, Navre M, Coffey RJ, Matrisian LM
(1991) Mol Carcinog 4: 527-33
MeSH Terms: Carcinoma, Colonic Neoplasms, DNA Probes, Gene Expression, Histocytochemistry, Humans, Matrix Metalloproteinase 10, Matrix Metalloproteinase 3, Matrix Metalloproteinase 7, Metalloendopeptidases, Nucleic Acid Hybridization, RNA, Messenger, RNA, Neoplasm, Stomach Neoplasms
Show Abstract · Added March 27, 2014
The expression of members of the family of matrix-degrading metalloproteinases (MMPs) is believed to contribute to the complex process of invasion and metastasis. In this study, specific cDNA probes for three members of the stromelysin subfamily of MMPs--stromelysin (MMP-3), stromelysin-2 (MMP-10), and pump-1 (MMP-7)--were used to examine the expression of these three different MMPs in human gastric and colonic carcinomas and in adjacent normal mucosa. The expression of pump-1 mRNA in malignant colon and stomach samples was striking. In a total of 10 gastric carcinoma samples examined, eight (80%) expressed pump-1 transcripts; similarly, 6 of 8 (75%) colon carcinoma samples were also positive. Stromelysin and stromelysin-2 mRNAs were not detected in any of these samples. Expression of the MMPs examined was not detected in any of the adjacent, grossly normal tissue samples. Using in situ hybridization and affinity purified anti-pump-1 antibodies, the expression of pump-1 mRNA and protein was localized to tumor cells and was not detected in stromal or lymphocytic cells. This data suggests that the inappropriate expression of pump-1 by malignant cells may contribute to the neoplastic phenotype.
1 Communities
1 Members
0 Resources
14 MeSH Terms