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)

Brown adipocyte respiration was measured in isolated cells from hypothyroid, hyperthyroid and euthyroid Sprague-Dawley male rats. Hypothyroidism was induced by providing drinking water containing methimazole and hyperthyroidism was induced by addition of thyroid powder to the diet. Brown adipose tissue (BAT) cells were isolated by collagenase digestion and oxygen consumption (VO2) was measured by Clark type oxygen electrodes. BAT cell respiration was stimulated by selective and nonselective beta-adrenergic agonists: BRL 35135A (BRL) and Isoprenaline (ISO). Basal BAT cells respiration did not differ according to thyroid status. Maximal VO2 responses of BAT adipocytes from hypothyroid rats were significantly lower than in euthyroidism after ISO and BRL. The reduced response was more marked for ISO than for BRL. The thermogenic sensitivity was significantly greater in euthyroid than is hypothyroid cells for ISO, but not for BRL. The euthyroid-hyperthyroid differences were not significantly different. These results suggest: basal respiration of BAT cells in hypo- and hyperthyroidism does not reflect the overall changes in whole body metabolism; the decreased thermogenic response in hypothyroidism might be due to decreased beta-adrenoceptor numbers and/or decreased intracellular thyroxine-triiodothyronine conversion; changes in sensitivity to ISO and BRL in vitro reflect the changes seen in VO2 in vivo.
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PMID:Brown adipose tissue cell respiration in hypo- and hyperthyroidism after stimulation with selective and non selective beta-adrenergic agonists. 168 47

Thyroid hormones influence Ca2+ homeostasis in both skeletal and cardiac muscle. Since secretory cells, like muscle cells, store and use Ca2+ in stimulus-response coupling, we have studied the effects of thyroid status on Ca2+ mobilization and secretion in a model secretory tissue, the pancreatic acinar cell. Hyperthyroidism was induced by rats by daily, subcutaneous injections of triiodothyronine for 8 days and hypothyroidism by adding 6-n-propyl-2-thiouracil to the drinking water for 14 days. Pancreatic acini were prepared by collagenase digestion of pancreatic tissue from hyper- and hypo-thyroid animals and from euthyroid controls. Ca2(+)-mobilization was assessed using Quin-2 fluorescence and secretion by assaying amylase release. The data indicate that the amount of Ca2+ mobilized by the muscarinic agonist carbachol or by cholecystokinin octapeptide increases with increasing thyroid hormone concentrations. Only in hypothyroidism was this change in Ca2+ homeostasis reflected by a parallel change in amylase secretion. This implies the existence of some compensatory mechanism which stabilizes secretory rate in the face of stimulus-evoked increases in intracellular Ca2+ concentration.
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PMID:Influence of thyroid status on Ca2+ mobilization and amylase secretion in rat pancreatic acini. 248 94

Hemidecortication, which consists of removing one cerebral hemisphere, leaving intact the thalamus and hypothalamus, affects the hypothalamus-hypophyseal axis producing hypothyroidism. Hemidecorticate rats showed a significant decrease in the weekly eruption rate of the upper incisors and partial recovery after the administration of thyrotrophin-releasing hormone (TRH). The uptake of [3H]-glycine, 1 and 4 h after a single injection, shown by radioautography, was 25 to 50 per cent higher in the periodontal ligament of the experimental animals. Most of the labelled material was non-collagenous proteins because only 20 to 30 per cent was removed by collagenase.
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PMID:The effects of cerebral hemidecortication on the eruption rate and uptake of [3H]-glycine by the periodontal ligament of the rat incisor. 315 Oct 48

Studies were carried out on the effect of triiodothyronine (T3) on the oxygen consumption of dispersed rat liver cells incubated for 2 hr at 37 degrees C. Thyroidectomized SD-NIH rats were kept on a low iodine diet with calcium chloride in the drinking water for 4 weeks or longer to assure hypothyroidism, verified by low serum thyroxine and T3 concentrations. Liver cells were obtained by portal vein perfusion with oxygenated collagenase-enriched Krebs-Ringer-bicarbonate buffer, after the method of Berry and Friend. Cell viability was evaluated by morphology, by trypan blue exclusion, and by biochemical parameters prior to 2-hr incubations with or without added hormone. The oxygen consumption of cell suspensions was measured with the Clark oxygen electrode after the 2-hr incubations at 37 degrees C with oxygenation of the flasks and alanine (5-10 mM) as substrate. In 31 experiments the oxygen consumption (QO2) was enhanced to 121% of control values with T3 in the medium at 3.3 nM ("physiological" level) and with an even greater effect (138% of control values) with 300-1000 nM T3 ("hyperthyroid" level). Cycloheximide at 100 microM was used to inhibit new protein synthesis by incubated hepatocytes. In 18 parallel experiments with cycloheximide blockade, no alteration of the stimulatory effect of T3 was evident. The results signify that incubated liver cells show an early response to thyroid hormone by extranuclear pathways that do not require new protein synthesis.
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PMID:Rapid thyroid hormone action in vitro in the absence of new protein synthesis. 653 49

The activity of type I 5'-deiodinase (5'DI) is known to correlate with thyroid status; it is high in hyperthyroidism and low in hypothyroidism. Recently, it was shown that the increased activity of type I 5'DI in hyperthyroidism is associated with an increase in enzyme contents as well as its mRNA in liver. However, it remains unknown whether thyroid hormone directly regulates the expression of 5'DI mRNA in hepatocytes. In this study, the direct actions of thyroid hormone as well as rT3 and dexamethasone on type I 5'DI mRNA were investigated using primary cultures of rat hepatocytes. Hepatocytes were prepared from euthyroid rats by collagenase perfusion and plated either on collagen-coated dishes for conventional monolayer cultures or on positively charged dishes for spheroid cultures. After hormonal treatments, the levels of mRNAs for type I 5'DI and albumin were determined by Northern blotting. In spheroid cultures, T3 increased type I 5'DI mRNA in a dose- and time-dependent manner, whereas the albumin mRNA level was not altered. A lesser effect was observed in hepatocytes cultured as monolayers. The T3-induced increase in 5'DI mRNA was not inhibited by pretreatment with cycloheximide, indicating that the effect of thyroid hormone on 5'DI mRNA is direct, not requiring de novo protein synthesis. rT3 did not affect the levels in type I 5'DI mRNA increased by T3. On the other hand, dexamethasone alone increased 5'DI mRNA and, when added together with T3, had a synergistic effect. In contrast to T3, dexamethasone increased albumin mRNA. Dexamethasone-induced increases in mRNAs for 5'DI and albumin were inhibited by pretreatment of cycloheximide. The present study indicated that T3 increases 5'DI mRNA through a direct action on its gene, whereas the effect of dexamethasone requires de novo synthesis of a protein factor(s).
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PMID:Effects of thyroid and glucocorticoid hormones on the level of messenger ribonucleic acid for iodothyronine type I 5'-deiodinase in rat primary hepatocyte cultures grown as spheroids. 824 26

Effects of thyroid hormone on proteoglycan degradation in various regions of cartilage were investigated. In propylthiouracil-treated rats with hypothyroidism, proteoglycan degradation in epiphyseal cartilage during endochondral ossification was markedly suppressed. However, injections of T(4) reversed this effect of propylthiouracil on proteoglycan degradation. In pig growth plate explants, T(3) also induced breakdown of proteoglycan. T(3) increased the release of aggrecan monomer and core protein from the explants into the medium. Accordingly, the level of aggrecan monomer remaining in the tissue decreased after T(3) treatment, and the monomer lost hyaluronic acid-binding capacity, suggesting that the cleavage site is in the interglobular domain. The aggrecan fragment released from the T(3)-exposed explants underwent cleavage at Glu(373)-Ala(374), the major aggrecanase-cleavage site. The stimulation of proteoglycan degradation by T(3) was less prominent in resting cartilage explants than in growth plate explants and was barely detectable in articular cartilage explants. Using rabbit growth plate chondrocyte cultures, we explored proteases that may be involved in T(3)-induced aggrecan degradation and found that T(3) enhanced the expression of aggrecanase-2/ADAM-TS5 (a disintegrin and a metalloproteinase domain with thrombospondin type I domains) mRNA, whereas we could not detect any enhancement of stromelysin, gelatinase, or collagenase activities or any aggrecanase-1/ADAM-TS4 mRNA expression. We also found that the aggrecanse-2 mRNA level, but not aggrecanase-1, increased at the hypertrophic stage during endochondral ossification. These findings suggest that aggrecanse-2/ADAM-TS5 is involved in aggrecan breakdown during endochondral ossification, and that thyroid hormone stimulates the aggrecan breakdown partly via the enhancement of aggrecanase-2/ADAM-TS5.
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PMID:Thyroid hormone enhances aggrecanase-2/ADAM-TS5 expression and proteoglycan degradation in growth plate cartilage. 1274 10