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)

A comparison was made between collagenase-dispersed guinea-pig atrial and ventricular tissues. Heparin containing cells were stained with alcian blue at pH 2.2, and counted by an automated technique (Technicon H6000). The cells were challenged with the specific antigen (ovalbumin), with antisera to guinea-pig IgG (non-subclass specific), IgG1 and IgG2, and the calcium ionophore A23187. Histamine release was measured by an automated spectrofluorometric technique, and leukotriene C4 was measured by radioimmunoassay. All of the following parameters were higher in the atrial than in ventricular cells (mean ratio and SEM of atrial: ventricular mast cell parameters in parenthesis): Histamine content/g wet tissues (3.32 +/- 0.71:1) (p less than 0.05), Absolute mast cell number as a proportion of total cell count (3.75 +/- 1.64:1), Histamine release induced by antigen (significant in one out of four experiments), anti-IgG (significant in three out of four experiments), anti-IgG1 (significant in two out of four experiments), and anti-IgG2 (higher but not statistically significant). Ionophore A23187 gave an inconsistent histamine release pattern: significantly higher release from atria in five treatments (different concentrations in different experiments), and higher ventricular release in three. Significantly more leukotriene C4 was released by antigen and the ionophore A23187 (mean of 3-5 treatments), but not with anti-IgG.
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PMID:Comparison of the response of mast cells in guinea-pig cardiac atria and ventricles. 243 72

Prostaglandin (PG) E and F output was studied in collagenase-dispersed amnion cells to determine the effect of extracellular Ca2+ upon PG synthesis. In the presence of 2.5 mM CaCl2, PGE and PGF output (picograms per 10(5) cells per 3 h) by cells obtained at term prior to labour following elective cesarean section (CS) was 183 +/- 39 and 127 +/- 23, respectively. This increased to 435 +/- 111 (p less than 0.025) and 241 +/- 49 (p = 0.056) from cells obtained after spontaneous labour and delivery at term (SL). Exclusion of CaCl2 from the medium (plus 0.1 mM EGTA) significantly reduced (p less than 0.025) PGE output in CS and SL cells (83 +/- 22 and 183 +/- 47, respectively) and PGF output in CS cells (70 +/- 17). PGE output in both CS and SL cells was unchanged when CaCl2 concentrations in the medium were decreased from 2.5 to 0.25 mM, but significantly attenuated (p less than 0.01) when extracellular CaCl2 was decreased from 0.25 to 0 mM. The voltage-sensitive Ca2+ channel blocker, D-600, decreased PGE output in the presence of (2.5 mM) CaCl2 to levels observed in the absence of CaCl2. Ionophore A23187 restored PGE output in the presence of D-600 and Ca2+. PGE output from CS amnion cells was stimulated by A23187 and elevated extracellular K+ (40 mM). In each case, exclusion of CaCl2 from the medium eliminated the response. These results suggest that PG output by human amnion is dependent, in part, upon the presence of extracellular Ca2+ and that Ca2+ may enter the cell via a potential-sensitive mechanism.
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PMID:Prostaglandin synthesis by human amnion is dependent upon extracellular calcium. 664 Apr 32