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)

The histamine-releasing effect of certain opiate drugs prompted a survey of endogenous opiates for mast cell-secretagogue activity. Since intestinal mucosal mast cells (MMC) differ from connective tissue mast cells in their response to a variety of secretagogues and anti-allergic compounds, we have examined the influence of several endogenous opiate peptides on histamine secretion from the two mast cell types in the rat. MMC hyperplasia was induced in rats infected with the nematode Nippostrongylus brasiliensis and MMC were isolated by collagenase digestion from the small intestine. Connective tissue mast cells from the peritoneal cavity (PMC) were isolated by peritoneal lavage. Dynorphin, alpha-neoendorphin, and beta-endorphin had a concentration-dependent secretagogue effect (10(-6)M to 10(-4)M) on PMC that was temperature and energy dependent, but MMC from the same animals were unresponsive to these agents. Differences between PMC and MMC did not appear to be attributable to the MMC isolation procedure since PMC treated similarly remained responsive to endorphin. Endorphin-induced histamine secretion from PMC was partially inhibited by the anti-allergic agent disodium cromoglycate. Inhibition with the opiate antagonist naloxone was nonspecific, occurring only at concentrations that also inhibited antigen-induced mediator release. Mast cell secretion induced by certain opiate peptides may therefore be nonreceptor mediated and relate to a direct membrane effect by basic peptides.
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PMID:The influence of endorphins on peritoneal and mucosal mast cell secretion. 620 30

This study examined the effects of an epithelial and a mesenchymal growth factor on pleural mesothelial cell proliferation and collagen synthesis, functions that may be important in the response of the pleura to injury. Epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) added singly caused significant increases relative to control in both the uptake of [3H]thymidine into the cellular DNA of subconfluent monolayers and of [3H]proline into collagenase-sensitive protein. Combinations of EGF and PDGF resulted in more than additive increases in proliferation and additive increases in collagen production relative to each factor alone. Media from control and growth factor-stimulated PMC demonstrated no gelatinase or collagenase activity, suggesting that the increase in net collagen production was secondary to enhanced synthesis. These data demonstrate that both epithelial and mesenchymal growth factors can stimulate PMC proliferation and collagen synthesis and that these growth factors have even greater effects when combined, particularly in regard to cellular proliferation. Increases in PMC proliferation and collagen synthesis in response to these growth factors may be important in healing the pleura after injury by a variety of disease processes.
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PMID:Growth factor modulation of rat pleural mesothelial cell mitogenesis and collagen synthesis. Effects of epidermal growth factor and platelet-derived factor. 820 47

The pleural mesothelial cell has a critical role in repairing the mesothelium after injury via its ability to produce connective tissue macromolecules. We have recently shown that proinflammatory cytokines and lipopolysaccharide induce pleural mesothelial cells to produce nitric oxide. The present study examined the effect of nitric oxide on pleural mesothelial cell protein synthesis. Rat pleural mesothelial cells were exposed to various combinations of tumor necrosis factor, interleukin-1, interferon-gamma, and lipopolysaccharide or to the nitric oxide donors: 6-morpholino-sydnonimine, S-nitroso-N-acetyl-D,L-penicillamine, sodium nitroprusside, and spermine-NO adduct for 24-48 h. Nitrate and nitrite (an index of nitric oxide production) and not collagen and noncollagen protein production (uptake of 3H-proline into collagenase-sensitive protein) were then determined. Net collagen production was significantly inhibited by the cytokine-lipopolysaccharide combinations tested. Collagen inhibition paralleled the time course of increased nitric oxide production. The inhibition of collagen production was also significantly reversed by the addition of NG-nitro-L-arginine methyl ester, and was reproduced by the addition of a 5:1 molar excess of L-arginine to NG-nitro-L-arginine methyl ester. Additionally, nitric oxide-generating compounds significantly inhibited collagen production in a dose-dependent manner compared to unexposed control cells. Net collagen production was inhibited to a greater degree than noncollagen protein synthesis. These results suggest that nitric oxide may be a significant mediator of PMC collagen production during conditions of significant pleural inflammation.
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PMID:Inhibition of pleural mesothelial cell collagen synthesis by nitric oxide. 889 63