Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.3 (collagenase)
 18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During cell proliferation, several "factors" are released into the microenvironment, or culture medium. The experiments described sought and examined agents that may cause or support malignant cell transformation. The response of colon cells from patients with ulcerative colitis (UC), familial polyposis coli (FPC) and colon carcinoma (CCC) to these agents was monitored by carcinoembryonic antigens (CEA) released into the medium during cell proliferation in a serum-free hormone-defined (SFHDM) medium, oncogenicity in athymic mice and colonigenicity, i.e. the ability of the cells to form colonies in soft agar. When cultured on the extracellular matrix (EM), i.e. footprints from colon carcinoma cells (short term or established cell lines), and in SFDHM, colon cells from patients with UC and FPC showed significant (P = 0.001) increases in all the three parameters. Analyses indicated that EM from cultures of [35S]methionine-labelled normal epithelial colon cells (NCE) differed from those left by UCC, FPC and CCC cell cultures. EM from NCE cell cultures did not contain [35S]methionine-labelled glycoproteins resistant to collagenase action which were not fragments of fibronectin, and which were present in EM from CCC cells. It is concluded that the extracellular matrix from malignant colon cells contains agents that support colon cell oncogenic transformation.
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PMID:Ulcerative colitis and familial polyposis oncologic transformation to colon carcinoma: changes in carcinoembryonic antigen release. 282 26

Glaucoma is a common cause of blindness affecting at least 66 million people worldwide. Pigmentary glaucoma is one of the most common forms of secondary glaucoma, and its pathogenesis remains unclear. Interleukin-18 (IL-18) is an important regulator of innate and acquired immune responses and plays an important role in inflammatory/autoimmunity diseases. Using the DBA/2J mouse as an animal model of human pigmentary glaucoma, we demonstrated for the first time that the expression of the IL-18 protein and gene in the iris/ciliary body and level of IL-18 protein in the aqueous humor of DBA/2J mice are dramatically increased with age. This increase precedes the onset of clinical evidence of pigmentary glaucoma, implying a pathogenic role of inflammation/immunity in this disease. We also observed that activated NF-kappaB and phosphorylated MAPK are increased in the iris/ciliary body of DBA/2J mice, suggesting that both signaling pathways may be involved in IL-18 mediated pathogenesis of pigmentary glaucoma in the eyes of DBA/2J mice. In addition, matrix metalloproteinase-2 (MMP-2) expression in the iris/ciliary body and the activity of MMP-2 in the aqueous humor are increased whereas tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) expression in the iris/ciliary body is decreased, indicating that the degradation process is involved in this mouse model of pigmentary glaucoma. Furthermore, the expressions of apoptosis-related genes, caspase-8, Fas, FADD, FAP, and FAF, and the activity of caspase-3 are increased in the iris/ciliary body of DBA/2J mice. Elucidation of biochemical and molecular mechanisms of IL-18 participation in the pathogenesis of pigmentary glaucoma should provide approaches for developing improved and targeted treatments to ameliorate this blinding disease. The possibility that altered IL-18 expression in the eye of DBA/2J mice initiates and/or amplifies the pathogenesis of pigmentary glaucoma requires further investigation.
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PMID:Involvement of inflammation, degradation, and apoptosis in a mouse model of glaucoma. 1598 30