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)

The effect of cadmium chloride (CdCl2) on cultured human vascular endothelial (HVE) cells and cultured human fibroblasts (HAIN-55 cells) was investigated. Umbilical vein-derived HVE cells were collected by enzymatic digestion with collagenase. At the concentration of 0-10 microM, Cd had hardly any effect on the cell viability of either cells. The viability of HVE cells decreased markedly at 100 microM, but not that of HAIN-55 cells. Morphologic examination by phase contrast microscopy revealed a more damaging effect of Cd on HVE cells than on HAIN-55 cells. These results suggest that Cd is more cytotoxic to HVE cells than HAIN-55 cells.
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PMID:Cadmium injury of cultured human vascular endothelial cells. 181 48

This study was designed to evaluate the role of neutrophils (PMNs) in the pathogenesis of emphysema. After administration of CdCl2 intratracheally to hamsters fed a lathyrogen, beta-amino propionitrile fumarate (BAPN), the classic lesions of emphysema developed. Administration of specific antineutrophil serum markedly reduced the PMN influx into the lungs which followed CdCl2 exposure and produced a substantial decrease in elastase and collagenase content of bronchoalveolar lavage fluid (BAL). The degree of emphysema in PMN-depleted hamsters given BAPN and CdCl2 was not different from that in hamsters given BAPN and CdCl2. Furthermore, the degree of acute lung injury following CdCl2, as determined by hydroxyproline content of BAL and by lung lipid peroxidation, was the same in PMN-depleted and non-depleted groups. Thus, PMNs were not necessary for the induction of emphysema in BAPN-CdCl2-treated hamsters. The results suggest that PMNs may not be obligate mediators of emphysema.
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PMID:The role of neutrophils in the development of cadmium chloride-induced emphysema in lathyrogen-fed hamsters. 299 Feb 23

1. Formation of inositol phosphates (InsPs) was measured in cross-chopped slices or dispersed cells, isolated by collagenase treatment, of guinea-pig ileum longitudinal smooth muscle pre-labelled with [3H]inositol. 2. Elevation of the extracellular K+ concentration by equimolar replacement of Na+ induced accumulation of InsPs in the dispersed cells and in the tissue slices. These effects were blocked by neither tetrodotoxin (1 microM) nor atropine (10 microM), and were approximately additive with carbachol-induced accumulation. 3. In the tissue slices, the response to K+ was partially inhibited by nifedipine (10 microM) and by CdCl2 (0.3 mM), but the carbachol-induced response was not altered. 4. Accumulation of InsPs induced by KCl-excess solution (high-K+ solution without Na+ replacement) was suppressed strongly by nifedipine and completely by CdCl2. The response to KCl excess was approx. 40% of that to high K+ with Na+ replacement. 5. Low-NaCl solution (replacement of NaCl with equimolar sucrose) also produced InsPs, and this was not blocked by either nifedipine (10 microM) or CdCl2 (0.3 mM). 6. The formation of InsPs by a maximally effective concentration of carbachol (1 mM) in the presence of KCl excess or low NaCl was greater than the additive effect of the two stimuli on their own. Enhancement of the carbachol-induced response by KCl excess disappeared in the presence of CdCl2 (0.3 mM). 7. These data suggest that formation of InsPs induced by high-K+ solution with equimolar replacement of Na+ consists of two components, i.e. high-K+-induced inositol-phospholipid hydrolysis by Ca2+ entry through voltage-sensitive channels, and low-Na+-induced formation of InsPs, insensitive to Ca2+ antagonists, but that both of them do not contribute significantly to the activation of phospholipase C by muscarinic stimuli.
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PMID:Lowering of the extracellular Na+ concentration enhances high-K+-induced formation of inositol phosphates in the guinea-pig ileum. 342 28

Nephrotoxicity is the major adverse effect produced by chronic exposure to cadmium (Cd). This injury is thought to be caused by the Cd-metallothionein complex (CdMT). In intact animals, CdMT is more efficiently taken up by the proximal tubules than CdCl2 and results in more renal damage. However, the mechanism(s) by which CdMT produces renal injury is not yet understood completely. Therefore, we used cultured renal proximal tubular cells to study the nephrotoxicity of CdMT and CdCl2. Rat kidney proximal tubules were isolated by collagenase perfusion, followed by percoll isopycnic centrifugation. 14C-alpha-methylglucose uptake and lactate dehydrogenase leakage were used as indices of nephrotoxicity. Surprisingly, CdMT was less toxic than CdCl2 to the cultured rat proximal tubule cells, as well as to cultured LLC-PK1 cells (a pig kidney proximal tubular cell line). Consistent with these observations on nephrotoxicity, 109CdMT uptake into these cultured renal cells was much less than that of 109CdCl2. Transwell cultures of LLC-PK1 cells were also used to examine the toxicity and uptake of CdCl2 and CdMT following basolateral and apical exposure. Uptake of both CdCl2 and CdMT from basolateral exposure was higher than that from apical exposure. Again, more 109CdCl2 was taken up and more cytotoxicity was observed in the CdCl2- than CdMT-exposed cells. In summary, CdCl2 is more toxic than CdMT to cultured rat kidney proximal tubules as well as LLC-PK1 cells. This is in contradiction to the greater in vivo nephrotoxic effects of CdMT than CdCl2. Therefore, cultured renal cells do not appear to be an appropriate model to study the nephrotoxicity of CdMT; transport of CdMT into proximal tubular cells in vivo does not appear to be maintained in vitro.
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PMID:Nephrotoxicity of CdCl2 and Cd-metallothionein in cultured rat kidney proximal tubules and LLC-PK1 cells. 794 May 41

The effect of cadmium chloride (Cd; CdCl2) on the tube formation by cultured human umbilical vascular endothelial cells (HUVEC) was examined. HUVEC were collected by enzymatic digestion with collagenase. Tube formation was studied by culturing the cells on a gelled basement membrane matrix (Matrigel). Treatment of HUVEC with 0.1 microM-1.0 mM Cd for 24 hours inhibited tube formation dose-dependently. The cadmium concentration inhibiting tube formation by 50% relative to untreated cells was about 150 microM. The length of tube formation decreased time-dependently with 150 microM Cd. The treatment of HUVEC by 50 nM of beta-phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C, increased tube formation. However, the inhibitory effect of Cd on tube formation was not affected by the addition of PMA. The pretreatment of the Matrigel by Cd inhibited tube formation similarly to the results of Cd treatment. These findings suggest that Cd inhibits the formation of a capillary network by HUVEC, and that the Cd-inhibitory effect on tube formation may have been dependent in this study on the degeneration of Matrigel by Cd.
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PMID:Cadmium injures tube formation by cultured human vascular endothelial cells. 918 55