Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.24.3 (collagenase)
18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum collagenase was significantly elevated in stage II, but not stage I sarcoidosis, in contrast to elevation of serum angiotensin-converting enzyme in stages I and II. Neither serum collagenase nor angiotensin-converting enzyme was elevated in active tuberculosis. Elevated serum collagenase and angiotensin-converting enzyme levels were decreased with steroid therapy. Serum collagenase and angiotensin-converting enzyme were significantly correlated but did not vary identically. Collagenase was not elevated in lymph nodes in sarcoidosis, in contrast to marked elevation of angiotensin-converting enzyme. The results suggest that serum angiotensin-converting enzyme is a more sensitive index of sarcoidosis activity than serum collagenase, which may have an ancillary role in assessment of the disease.
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PMID:Serum and lymph-node collagenase in sarcoidosis. Comparison with angiotensin-converting enzyme. 21 44

To test the hypothesis that idiopathic pulmonary fibrosis (IPF) is mediated through collagenase present in the lower respiratory tract, we used the fiberoptic bronchoscope to obtain fluid from the lower respiratory tract of 24 patients with IPF, 18 controls and nine patients with sarcoidosis. The fluid was analyzed for a variety of enzymes, including collagenase. Fifteen of 21 patients with IPF showed collagenase activity, whereas normal controls and patients with sarcoidosis showed none (P greater than 0.001, for all comparisons). In two patients with IPF who were re-evaluated after eight to 24 months, the collagenase activity was persistent. Fluid from patients with IPF also contained elevated levels of a non-specific neutral protease (P greater than 0.01 compared with controls), but there was no elastase activity in fluid from patients with IPF or from controls. The collagenase found in lavage fluid in IPF cleaved lung collagen into collagenase-specific TCA and TCB fragments. We conclude that in IPF the collagen of the lung is subjected to sustained lysis, followed by disordered resynthesis, and that the presence of active collagenase in the lower respiratory tract is a specific feature of the alveolitis associated with this disease.
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PMID:Collagenase in the lower respiratory tract of patients with idiopathic pulmonary fibrosis. 22 66

The processing of precursor interleukin 1 beta (IL1 beta) by elastase, cathepsin G, and collagenase, the major proteases released at sites of inflammation, was investigated using recombinant pro-IL1 beta. Each of these proteases cleaved the 31-kDa inactive precursor to a form similar in size and specific activity (greater than 10(8) units/mg) to the 17-kDa mature protein isolated from activated monocytes. Elastase, collagenase, and cathepsin G cleaved the IL1 beta precursor at distinct sites which are amino-terminal to the monocyte-processing site, Ala-117 (Cameron, P., Lumjuco, G., Rodkey, J., Bennett, C., and Schmidt, J. A. (1985) J. Exp. Med. 162, 790-801). Amino-terminal sequencing of the products of digestion by elastase and cathepsin G determined that resultant active IL1 beta proteins contained an additional 13 or 3 amino acids relative to mature IL1 beta. Synovial fluid collected from patients with inflammatory polyarthritis and bronchoalveolar lavage fluid from patients with sarcoidosis supplied similar processing activity(s). Control fluids from patients who had no symptoms of inflammatory disease did not exhibit processing activity. Lavage fluids that processed precursor IL1 beta were demonstrated to contain cathepsin G and/or elastase activity, whereas controls were negative. Because a significant fraction of IL1 beta may be secreted from monocytes as the inactive 31-kDa precursor (Hazuda, D. J., Lee, J. C., and Young, P. R. (1988) J. Biol. Chem. 263, 8473-8479, Bomford, R., Absull, E., Hughes-Jenkins, C., Simpkin, D., and Schmidt, J. (1987) Immunology 62, 543-549, and Mizel, S. B. (1988) in Cellular and Molecular Aspects of Inflammation Poste, G., and Crooke, S., eds) pp. 75-93, Plenum Publishing Corp., New York), these results suggest that in vivo the IL1 beta precursor can be processed after secretion by any of several proteases released at inflammatory sites.
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PMID:Processing of precursor interleukin 1 beta and inflammatory disease. 215 47

To assess the usefulness of bronchoalveolar lavage (BAL) collagenase measurement in gauging disease severity and outcome in sarcoidosis, we analyzed BAL fluids from 84 patients with sarcoidosis for collagenase and monitored disease progress in these patients for a minimum of 12 months. Twenty patients (24%) were found to have BAL collagenase activity on initial evaluation (collagenase-positive group). Compared with patients without BAL collagenase (collagenase-negative group), the collagenase-positive group had (1) a higher proportion of BAL suppressor T cells (p less than 0.03); (2) a lower helper-suppressor T-cell ratio (p less than 0.002); (3) lower mean percent predicted FEV1, FVC, and DLCO levels (p less than 0.05); and (4) a higher proportion of patients with advanced (Stage 4) disease on chest roentgenogram (p less than 0.001). Significant differences were also observed between the collagenase-positive and collagenase-negative groups during follow-up. A higher proportion (55%, n = 11) of collagenase-positive patients required corticosteroid therapy than did collagenase-negative patients (26%; n = 17; p less than 0.025). Of those who remained untreated, pulmonary function tended to decrease in the collagenase-positive group, whereas mean pulmonary function levels actually improved in the collagenase negative group (p less than 0.05). Of those who required therapy, mean percent predicted FVC and DLCO levels improved significantly after treatment in the collagenase-negative group (p less than 0.01 and p less than 0.05, respectively), whereas an improvement in percent predicted FVC levels only (p less than 0.01) was observed in the collagenase-positive group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulmonary disease progress in sarcoid patients with and without bronchoalveolar lavage collagenase. 216 22

To better understand how the activity of inflammatory cells collected by bronchoalveolar lavage (BAL) could affect the outcome of granulomatous and fibrotic pulmonary diseases, we studied secretory products and messenger ribonucleic acid (mRNA) expression for certain cytokines of BAL cells in 10 controls, 14 patients with interstitial pulmonary fibrosis (IPF) and 22 patients with sarcoidosis. We assayed the activity of 48 h conditioned media for: 1) their biological action on fibroblast proliferation and prostaglandin E2 (PGE2), collagenase and collagen production by fibroblasts; 2) TNF alpha levels by bioassay and radioimmunoassay; 3) interleukin 1 (IL-1) alpha and beta and beta levels by solid phase enzyme immunoassay (EIA); 4) tumor necrosis factor (TNF) and IL-1 inhibitory activity. We also measured, in freshly isolated BAL cells: 1) mRNA levels for IL-1 alpha and beta and TNF alpha; 2) cell-associated IL-1 alpha and beta by EIA. The only difference found in the assessment of the biological activity of BAL cells conditioned medium was an increase in fibroblast proliferation in sarcoidosis vs IPF patients. The IL-1 alpha and beta, and TNF alpha contents of conditioned media were similar in the three groups. Inhibitory activity against IL-1 and TNF alpha was found in a few patients. Further analysis revealed two peaks of inhibitory activity against IL-1 (20-25 kD and 35-40 kD), as well as a distinct TNF alpha inhibitory activity which could be retained on a TNF alpha-binding affinity column. No mRNA expression for TNF alpha was found in freshly isolated BAL cells, whereas very variable levels of IL-1 alpha and beta mRNA levels were detected in the three groups. Because of these variable results of differences in functional state between freshly isolated and cultured BAL cells, and of the presence of inhibitory substances against IL-1 and TNF alpha, it is unlikely that the development of fibrosis could be ascribed to a single disorder or abnormality.
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PMID:Fibroblast-alveolar cell interactions in sarcoidosis and idiopathic pulmonary fibrosis: evidence for stimulatory and inhibitory cytokine production by alveolar cells. 219 8

We studied collagenase, gelatinase and stromelysin syntheses by human fibroblasts cultured on three models of tridimensional matrix: native collagen sponge, native collagen complexed with glycosaminoglycans sponge, and acellular sarcoid matrix complex prepared from human sarcoid granulomas. Collagenase and stromelysin biosyntheses were differently stimulated according to culture conditions. Fibroblasts secreted a same amount of collagenase or stromelysin when cultured on collagen and collagen-glycosaminoglycans sponges, while collagenase and stromelysin secretions were widely amplified when cultured on sarcoid matrix complex. In contrast, gelatinase production was equally induced by the three culture conditions. In the different culture conditions on tridimensional matrix, the three matrix metalloproteinases were synthesized in a latent form. Thus, the sarcoid matrix complex stimulated the release of collagenase and stromelysin by fibroblast, but did not stimulate the release of gelatinase. This suggests that collagenase and stromelysin syntheses are co-regulated while gelatinase production is controlled by a distinct mechanism.
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PMID:Interstitial collagenase (MMP-1), gelatinase (MMP-2) and stromelysin (MMP-3) released by human fibroblasts cultured on acellular sarcoid granulomas (sarcoid matrix complex, SMC). 255 5

Bronchoalveolar lavage fluid from 43 patients with biopsy proved sarcoidosis and 10 control subjects were assayed for fibronectin and collagenase activity. Fibronectin was significantly increased in the group with sarcoidosis and was found to be positively correlated with angiotensin converting enzyme activity, protein concentration, percentage of T cells and helper:suppressor ratios in the lavage fluid. Increased fibronectin in the bronchoalveolar lavage fluid was not related to functional or radiographic indices of interstitial disease and did not identify patients subsequently requiring treatment. Latent collagenase was present in bronchoalveolar lavage fluid from 16 patients with sarcoidosis but not in any control sample. There was no association between the collagenase activity and the cell profiles of the lavage fluid. Yet carbon monoxide transfer factor was decreased in patients with bronchoalveolar lavage fluid collagenase. Ten of 16 patients with bronchoalveolar lavage fluid collagenase had radiographic class III or IV disease and a disease duration of more than two years. On follow up 62% of patients with bronchoalveolar lavage fluid collagenase required subsequent treatment, compared with only 23% of patients without collagenase. These results indicate an association between bronchoalveolar lavage fluid collagenase and progressive, prolonged disease in sarcoidosis, whereas increased bronchoalveolar lavage fluid fibronectin is associated with indices of disease activity.
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PMID:Collagenase and fibronectin in bronchoalveolar lavage fluid in patients with sarcoidosis. 284 27

The clinical course of sarcoidosis is varying and unpredictable. Once the diagnosis has been made, the clinician needs simple tests to detect and predict remission or progression, to determine whether treatment is effective or not, and to assess the clinical activity of the disease. Sarcoidosis is a multisystem disease, but the lungs are almost always involved. Traditionally, the clinical management has therefore included chest X-rays and lung function studies. Extrapulmonary lesions have been followed in different ways. Sensitive and reproducible biochemical tests would be helpful in evaluating the clinical course of patients with sarcoidosis, if they measure functions related to the granulomatous inflammation. This review will deal with measurements of serum and urinary calcium, and 1,25-dihydroxyvitamin D. The usefulness of single and serial determinations of lysozyme, angiotensin converting enzyme, beta 2-microglobulin, collagenase, carboxypeptidase and glucuronidase in serum, bronchoalveolar lavage fluid, and other biological fluids will be discussed.
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PMID:Biochemical markers in sarcoidosis. 302 7

In this review we have surveyed recent investigations of early cellular events in pulmonary fibrosis both in animal models and in human diseases. Analysis of the interactions of the numerous cell types in the lung following injury is an almost overwhelmingly complex enterprise. In the animal models experimental design has a profound effect on results, making it difficult to compare studies when species, fibrogenic agent, dose, route of exposure, schedule of administration, time course, and analytical methods may not be equivalent. In human diseases we are rarely able to obtain data at precisely the same time point in the course of the disease even among patients in the same study, and possible confounding variables present are legion. Transcending these difficulties for the moment, can we draw any conclusions from our current knowledge of early cellular interactions in pulmonary fibrosis? What is striking is not that there are so many agents that can potentially induce pulmonary fibrosis, but that the lung has such capabilities for recovery. Although the major effector cells may all initially participate in damaging the lung and initiating fibrosis, there is evidence that they may also have the capacity to participate in subsequent repair. Macrophages may initially recruit fibroblasts and stimulate them to proliferate, only to suppress them subsequently. Macrophage production of prostaglandins can lead to suppression of macrophage, neutrophil and lymphocyte responses, thus attenuating tissue injury and the development of fibrosis. Neutrophils may initially release toxic metabolites and enzymes that damage parenchyma. However, there is evidence that they may later play a role in attenuating fibrosis, perhaps through collagenase secretion, or through as yet unknown mechanisms. Lymphocytes may initially participate in a number of damaging ways by secreting chemoattractants for other cells and participating in destructive autoimmune processes. However, there is evidence that subpopulations of T cells may dramatically shift during the course of fibrosis, leading to attenuation of the process. It may thus be useful to consider irreversible pulmonary fibrosis as the end result of a process in which the balance of normal injury/repair mechanisms is disrupted. There is clearly no single "fibrogenic event." Rather, there seem to be a number of places where disruption of balance/repair processes may begin. In diseases of unknown etiology such as sarcoidosis or IPF, loss of control may occur at the genetic level, leading to the destructive alveolitis that is the apparent precursor of fibrosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Early cellular events in pulmonary fibrosis. 352 17

The diagnostic evidence of the ACE and CP activity alone is limited with regard to the specifity of sarcoidosis. In connection with the X-ray diagnostics and the histological ascertainment the determination of the two enzyme activities, however, is an enrichment of the programme of diagnostics. High ACE- and CP-values speak for the presence of numerous sarcoidosis granulomas and for the affection of many organs, respectively, when the sarcoidosis is ascertained. This fact is valuable in the diagnostics of sarcoidosis of the myocardium. For therapy controls or investigations of the course of the disease the two enzymes are to be used, since they give references to the activity of the disease. In this case the sensitivity of the ACE-determination seems to be larger than that one of the collagen peptidase.
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PMID:[Determination of enzyme activity in sarcoidosis--comparison of angiotensin convertase and collagen peptidase]. 609 47


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