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)

Oral submucous fibrosis (OSF) is characterized by an abnormal accumulation of collagen fiber in oral submucosa. OSF is a collagen disease and is also regarded as a precancerous lesion. In the previous study, we discovered that the collagen content in oral mucosa of OSF is statistically higher than in normal mucosa. This research examined the relationship between the fibrosis and collagenase activity. Collagenase activity was determined by using soluble 14C-glycine-labeled collagen (9813 cpm/200 micrograms/tube) as a substrate in a solution incubated for 30 hours at 35 degrees C. The results showed that the collagenase activity of the OSF was much lower than that of normal oral mucosa (65.23 +/- 19.49 units/g tissue in normal mucosa vs. 29.48 +/- 5.69 units/g tissue in OSF). Furthermore, the cleavage pattern revealed by SDS-Polyacrylamid gel electrophoresis (SDS-PAGE) confirmed that the partially purified OSF collagenase was likely to be typical mammalian collagenase, with a molecular weight of about 68.0 kDa.
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PMID:Collagenase activity in oral submucous fibrosis. 149 4

Oral submucous fibrosis (OSF) is a chronic fibrotic disease of the oral cavity and oropharynx characterized by fibroelastic change in the mucosa which leads to progressive inability to open the mouth. The inflammatory cells in the lesional tissue consist mainly of T lymphocytes, with a high CD4:CD8 ratio, and major histocompatibility complex (MHC) class II expressing antigen-presenting cells. Cytokines and growth factors produced by inflammatory cells within the lesion may promote fibrosis by inducing proliferation of fibroblasts, upregulating collagen synthesis and downregulating collagenase production. The authors used a three-stage immunoperoxidase technique to investigate the expression of interleukin alpha (IL-1alpha) and beta, IL-6 interferon (IFN)-alpha, beta and gamma, transforming growth factor beta (TGF-beta), platelet-derived growth factor (PDGF) and basic fibroblast growth factor (bFGF) in frozen sections of OSF and compared it with that in normal buccal mucosa. The expression of cytokines and growth factors in normal tissues was consistent with their well known distribution and cell of origin, but the intensity and distribution in OSF were all, with the exception of IFN-alpha and gamma, upregulated with strong expression in both the epithelium and underlying connective tissue. IFN-alpha showed a similar pattern of staining in both normal mucosa and OSF. IFN-gamma showed little or no expression in most lesional tissues, suggesting an innate deficiency or downregulation of this cytokine. The general increase in pro-inflammatory cytokines and growth factors, and reduced production of IFN-gamma, may play an important role in the pathogenesis of OSF.
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PMID:Immunolocalization of cytokines and growth factors in oral submucous fibrosis. 977 Mar 33

Oral submucous fibrosis (OSF) is a precancerous condition of the oral cavity. It is a collagen-related disorder induced by betel quid chewing, a habit that is common in Taiwan. However, the cumulative exposure to betel quids varies in OSF patients. It seems that there is individual susceptibility to betel quid-induced OSF. This study compared the association of OSF and polymorphisms of six collagen-related genes, collagen 1A1 and 1A2 (COL1A1 and COL1A2), collagenase-1 (COLase), transforming growth factor beta1 (TGF-beta1), lysyl oxidase (LYOXase), and cystatin C (CST3), between patients with low and high exposure to betel quids. A total of 166 patients with OSF from a medical center and 284 betel quid chewers who were free of OSF and oral cancer, from the same hospital and five townships, were recruited. PCR-based restriction fragment length polymorphism assays were used to determine the genotypes of the six collagen-related genes situated on different chromosomes. We found that the genotypes associated with the highest OSF risk for collagen 1A1, collagen 1A2, collagenase-1, transforming growth factor beta1, lysyl oxidase, and cystatin C were CC, AA, TT, CC, AA, and AA, respectively, for the low-exposure group, and TT, BB, AA, CC, GG, and AA, respectively, for the high-exposure group. A trend was noted for an increased risk of OSF with increasing number of high-risk alleles for those with both high and low exposures for betel quid. The cell selection mechanism of oral fibroblasts is proposed to explain the effect of the modification of cumulative betel quid exposure on the risk profiles of collagen-related genes. These results imply that susceptibility to OSF could involve multigenic mechanisms modified by the betel quid-exposure dose.
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PMID:Interaction of collagen-related genes and susceptibility to betel quid-induced oral submucous fibrosis. 1210 Nov 12

Oral submucous fibrosis is a chronic, progressive scarring disease associated with both significant morbidity including pain and limited mouth opening and an increased risk for malignancy. This systematic review evaluated the different medicinal (i.e. nonsurgical) interventions available for the management of oral submucous fibrosis. An automated literature searches of online databases from January 1960 to December 2013 were performed and only studies with high level of evidence based on the guidelines of the Oxford Centre for evidence-based medicine were selected. Thirteen studies (3 randomized controlled trials and 10 clinical trials/controlled clinical trials) were included and drugs like steroids, hyaluronidase, human placenta extracts, chymotrypsin and collagenase, pentoxifylline, nylidrin hydrochloride, iron and multivitamin supplements including lycopene were used. There is a clear lack of evidence on the available drug treatment for oral submucous fibrosis and further high quality randomized controlled trials are needed to evaluate the different therapeutic agents.
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PMID:Evaluation of medicinal interventions for the management of oral submucous fibrosis: a systematic review of the literature. 2582 14