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)

Collagen synthesis in normal BHK 21/cl 13 and chemically transformed temperature sensitive BHK 21/cl 13 cells (Me2N4) was assessed by examination of hydroxyproline formation and collagenase-susceptible protein. The Me2N4 cells lost their ability to synthesize collagen at both permissive and nonpermissive temperatures for transformation. These conclusions were confirmed by polyacrylamide-gel eletrophoresis and CM-cellulose chromatography. Prolyl hydroxylase activity was present in both normal and transformed cells even when no collagen could be demonstrated. The production of noncollagen protein, although decreased in the transformed cell, did not change as drastically as the collagen synthesis.
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PMID:Collagen synthesis in normal BHK cells and temperature-sensitive chemically transformed BHK cells. 22 63

The contribution of collagen degradation, as measured by collagenase activity, to the accumulation of collagen during hepatotoxic fibrogenesis was examined using a carbon tetrachloride rat model. Both active and inactive enzyme forms were determined with the inactive form quantitated following activation by limited trypsin digestion of the liver homogenate. The rate of collagen biosynthesis was monitored by quantitating hepatic prolyl hydroxylase activity and accumulation of collagen. In one study CCI4 was administered twice weekly, i.p. (0.2 mL, 33% v/v in light mineral oil) for sixteen weeks, with animals sacrificed every two weeks. Histologic examination of liver sections and serum alanine transaminase levels indicated a progressive necrosis and fibrosis which was confirmed by the increase in hepatic hydroxyproline content from 0.303 to 4.84 micrograms/mg wet wt. tissue. Prolyl hydroxylase activity increased in a time dependent manner to a maximum of 3.7 X control. This increase was accompanied by a large increase in both active collagenase (15.0-40.8 mU/g protein) and latent collagenase activity (69.8-191.7 mU/mg protein). These increases were maintained through the transition to irreversible fibrosis. The increase in active collagenase activity was positively correlated with collagen content. A second short term CCI4 treatment study confirmed a transient alteration in the active to latent collagenase ratio early in the fibrotic process. These results demonstrate the dynamic changes in hepatic collagenase levels and indicate that the fibrotic lesion is not dependent on decreased collagenase levels for collagen accumulation.
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PMID:Hepatic collagenase activity during carbon tetrachloride induced fibrosis. 630 97

The pathogenesis of chronic pancreatitis (CP) has been debated as to whether it is a de novo process or the consequence of acute pancreatitis (AP). We investigated whether recurrent AP in rats leads to CP, by sequential morphological and biochemical studies. Thirty male Wistar rats were fed a choline-deficient diet with intraperitoneal ethionine injections twice daily at a dose of 60 mg/100 g body weight twice weekly, and six rats were killed at 4, 6, and 8 weeks; the remaining 12 rats, followed without further treatment, were killed at 12 and 16 weeks. The pancreata from study and control groups were examined by histology, immunohistochemistry, and bio- and immunoassays. Histologically, moderate to severe intra- and perilobular fibrosis and other CP-like lesions appeared maximally at 8 weeks. Immunohistochemically, the earliest extracellular matrix change was strong fibronectin staining at 4 weeks, with a progressive increase to 8 weeks. Collagens I and III came to show strong, and collagen IV moderate, interstitial staining at 6-8 weeks. These morphological changes, however, returned to nearly normal at 16 weeks. Prolyl hydroxylase was significantly elevated at 4 and 6 weeks and normalized after 8 weeks, with no significant change in collagenase. In conclusion, our results suggest that even severe CP-like lesions induced by recurrent AP are reversible in the absence of persistently elevated prolyl hydroxylase and/or suppressed collagenase. The mechanism regulating these changes remains to be studied further.
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PMID:Does recurrent acute pancreatitis lead to chronic pancreatitis? Sequential morphological and biochemical studies. 916 78