Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Expression of the Na(+)-K(+)-adenosinetriphosphatase (ATPase) gene family in rat intestinal epithelial cells was examined using RNA blot hybridization analyses. Rat intestinal epithelial cells express only the alpha 1- and beta 1-subunit mRNAs. A gradient in expression of alpha 1- and beta 1-subunit mRNA was seen along the villus-crypt unit in both jejunum and ileum, i.e., villus tip >> crypt cells. Regional differences in expression were observed along the intestine. alpha 1- and beta 1-subunit mRNA abundance was similar in jejunum, ileum, and colon while enzymatic activity was highest in the jejunum and lowest in the ileum. Administration of thyroid hormone to thyroidectomized rats increased the expression of alpha 1- and beta 1-subunit mRNAs in jejunum but not in colon. Hypothyroidism had no effect on subunit mRNA expression. The human intestinal cell line Caco-2 was also studied. These cells also expressed only the alpha 1- and beta 1-isoform mRNAs and demonstrated a developmental profile in both mRNA and enzymatic activity. Furthermore, in Caco-2 cells both alpha 1- and beta 1-mRNAs and Na(+)-K(+)-ATPase enzymatic activity were stimulated by thyroid hormone. Caco-2 cells transfected with 5' flanking regions of the human Na(+)-K(+)-ATPase beta 1-gene linked to the chloramphenicol acetyltransferase (CAT) reporter gene responded to 3,5,3'-triiodothyronine (T3) treatment with increased expression of CAT activity. This suggests that the 5' flanking region of the beta 1-gene contains a thyroid hormone response element and that T3 upregulation occurs at the transcriptional level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Na(+)-K(+)-ATPase gene expression in rat intestine and Caco-2 cells: response to thyroid hormone. 823 61

The incorporation of 32Pi into phosphatidylinositols and inositol trisphosphates was studied in Langendorff-perfused hearts from hypothyroid, euthyroid and hyperthyroid rats. The hearts were perfused with modified Krebs buffer containing [32P]orthophosphate and the degree of 32P-labeling of phosphatidylinositol, phosphatidylinositol 4-monophosphate, phosphatidylinositol 4,5-bisphosphate, inositol trisphosphates and phosphatidic acid was measured. Hyperthyroidism was associated with increases in rates of rise and fall of left ventricular systolic pressure, sarcoplasmic reticular Ca(2+)-ATPase activity and 32P-labeling of phosphatidylinositols, inositol trisphosphates and phosphatidic acid. These measurements were significantly decreased in hypothyroid hearts. The tissue levels of inositol 1,4,5-trisphosphate isoform were found to be significantly higher in hyperthyroid hearts and lower in hypothyroid hearts than in euthyroid ones. Examination of phosphoinositide-specific phospholipase C activity in the perfused hearts revealed that hyperthyroidism was associated with an increase in the membrane-associated enzymatic activity, assayed at physiological calcium concentrations, while hypothyroidism was associated with a decrease in this activity as compared with control hearts. These findings indicate that alterations in the thyroid state of the myocardium may be associated with changes in basal phosphoinositide turnover which may contribute to alterations in myocardial contraction.
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PMID:Effect of thyroid status on phosphatidylinositols in rat heart. 829 67

Thyroid hormones control the expression of genes coding for myosin isoforms, the Na-K ATPase pumps and the Ca-ATPase canals of the sarcoplasmic reticulum. This explains the increase of contractility and relaxation of skeletal muscles observed in hyperthyroidism, as opposed to hypothyroidism. Control of key-enzymes of the main energetic pathways accounts for inhibition of oxidative metabolisms in hypothyroidism and excessive glycolysis recruitment in hyperthyroidism. In both cases muscle performance is reduced, with accumulation of lactic acid at exercise. This is due to defective pyruvate oxidation and proton expulsion in hypothyroidism, and to acceleration of glycolysis in hyperthyroidism. These abnormalities partly explain why subjects with dysthyroidism are intolerant to exertion.
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PMID:[Control of muscular bioenergetics by the thyroid hormones]. 831 32

To assess the effects of hypothyroidism (HT) on small-intestinal function, HT was induced in rats (120-150 g) by methimazole in drinking water. After 6 wk of methimazole, intestinal absorption studies were performed in HT and in control (C) rats by in situ luminal perfusion of a 20-cm proximal jejunal loop with a bicarbonate buffer containing sodium, glucose or fructose, glycine or lysine, and phenol red as a nonabsorbable marker for determination of water fluxes. Mucosa from the perfused segment was taken for assay of disaccharidases and ATPases and for light and electron microscopy. Compared with C rats, HT rats had significantly lower jejunal transport rates of water (2.54 +/- 0.36 versus 5.02 +/- 0.7 microL/min/microgram mucosal protein, p < 0.03), sodium (37.1 +/- 10.3 versus 102.7 +/- 18.6 mumol/min/microgram protein, p < 0.05), and glucose (1.49 +/- 0.28 versus 5.17 +/- 0.82 mumol/min/microgram protein, p < 0.02). A reduction in glycine transport was also observed but did not attain statistical significance (p = 0.058). Fructose and lysine transport was unchanged. Mucosal sucrase and lactase activities were similar in both groups, but Na,K-ATPase was significantly lower in HT rats (1.17 +/- 0.3 versus 4.03 +/- 1.5 mumol inorganic phosphate/h/mg protein; p < 0.05), with a diminution of ouabain binding sites by 41.5%. Light microscopy of jejunal mucosa from HT rats did not differ from that from C rats; electron microscopy showed mild mitochondrial swelling in HT enterocytes. A group of HT rats were treated with L-thyroxine during 4 wk; these rats had absorption rates, mucosal enzyme activities, ouabain binding, and mucosal morphology not different from C rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of hypothyroidism on jejunal mucosal function: study by in situ luminal perfusion in rats. 839 45

Specific activities of prostatic phosphomonoesterases (acid and alkaline phosphatases) and adenosine triphosphatases (Mg2+, Ca2+ and Na+/K+ dependent ATPases) were studied in albino rats, under altered thyroid hormone status. Thyroidectomy induced hypothyroidism decreased the specific activities of acid and alkaline phosphatases, Na+/K+ and Ca2+ dependent ATPases in ventral prostate. Hyperthyroidism (25 micrograms thyroxine/100g body weight/day for 60 days, im) enhanced the activities of acid phosphatase and Na+/K+ dependent ATPase, while Ca2+ dependent ATPase decreased. The altered thyroid status had no effect on the activity of ventral prostatic Mg2+ dependent ATPase. The data obtained in the present study showed differential and specific responses of various ventral prostatic phosphatases to the hypo or hyperthyroid status. The study also shows the necessity of an optimum level of thyroid hormones to maintain the normal activities of these enzymes and their secretory function in ventral prostate.
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PMID:Ventral prostatic phosphomonoesterases and adenosine triphosphatases in hypo- and hyperthyroid albino rats. 839 67

In order to examine the influence of thyroid hormones on the postnatal development of cardiac excitation-contraction coupling, newborn rats were made hypo- or hyperthyroid, and several key factors involved, directly or indirectly, in Ca2+ signaling: L-type Ca2+ channels (1,4-dihydropyridine receptors), Ca(2+)-release channels of sarcoplasmic reticulum (ryanodine receptors), beta-adrenoceptors, thapsigargin-sensitive Ca(2+)-ATPase and Na(+)-K(+)-ATPase (enzyme activity and ouabain receptors), were investigated in membrane fractions from ventricular tissue, collected on day 21. Hypothyroidism induced a moderately lower myocardial density of 1,4-dihydropyridine and ryanodinerece receptors (reduced by 23% and 31%, respectively, with respect to euthyroid controls), and much reduced levels of beta-adrenoceptors, Ca(2+)-ATPase and Na(+)-K(+)-ATPase activities. Hyperthyroidism induced only a moderate (22%) decrease in the myocardial density of 1,4-dihydropyridine receptors and a marked (240%) increase of the alpha 2 isoform of Na(+)-K(+)-ATPase. To analyse the subsarcolemmal localization of L-type channels, microsomal fractions were subfractionated by density equilibration in sucrose gradient. In gradients from control and hyperthyroid rats, most 1,4-dihydropyridine receptors were recovered in high-density subfractions, their distribution following that of ryanodine receptors, whereas, in gradients from hypothyroid rats, most 1,4-dihydropyridine receptors were recovered in low-density subfractions, together with beta-adrenoceptors and Na(+)-K(+)-ATPase. We conclude that thyroid hormones are important for the postnatal changes in the myocardial density of several channels and pumps involved in Ca2+ fluxes, as well as for the postnatal redistribution of L-type Ca2+ channels from non-junctional sarcolemma to junctional structures, a key process for the efficient operation of excitation-contraction coupling in adult ventricular tissue.
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PMID:Influence of thyroid status on postnatal maturation of calcium channels, beta-adrenoceptors and cation transport ATPases in rat ventricular tissue. 852 34

Skeletal muscle is one of the major target organs for thyroid hormone. The muscles most commonly affected are those used during prolonged effort (slow-twitch muscles). One of the major clinical features is the shortening of the Achilles-tendon reflex time in hyperthyroidism and its prolongation in hypothyroidism. Most of the peripheral effects of the thyroid hormones can be ascribed to the action of triiodothyronine (T2), which is produced by de-iodination of thyroxine (T4) in liver and kidney. From the plasma, T3 is actively transported into skeletal muscle. The Ca2+ ATPase in skeletal muscle is responsible for removal of Ca2+ ions from the cytosol into the sarcoplasmic reticulum (SR) during relaxation, and the Na+, K+ ATPase in the plasma membrane is responsible for restoration of the membrane potential after excitation. The concentrations of Ca2+ ATPase and Na+, K+ ATPase in rat skeletal muscle have been shown to increase four- and 10-fold, respectively, in the transition from the hypothyroid to the hyperthyroid state. In humans, a linear correlation between the Na+, K+ ATPase concentration of skeletal muscle and the free T4 index was established. Significant effects of T3 on Ca2+ ATPase and Na+, K+ ATPase can be detected 24 h after a single injection. These effects are mediated by increased production of mRNA for the respective proteins, initiated by binding of T3 to nuclear receptors. Passive fluxes of Ca2+, Na+ and K+ also show a significant rise after T3 treatment. The increase in passive fluxes of Na+ and K+ can be detected before the rise in the concentration of Na+, K+ ATPase, suggesting that T3. In addition to its nuclear effects, may have a direct effect on the plasma membrane. Apart from their significance for muscle function in thyroid disease, the changes in Ca2+ ATPase and Na+, K+ ATPase will be important in other conditions where T3 and T4 levels show dramatic changes, i.e. during postnatal development, starvation and undernutrition, as well as in non-thyroidal illness (low-T3 syndrome).
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PMID:Effects of thyroid hormones on contractility and cation transport in skeletal muscle. 872 93

This study examined the influence of experimental hypothyroidism on myosin isoform distribution and contractile function of the costal diaphragm. Adult female Sprague-Dawley rats were randomly assigned to control (n = 12) or hypothyroid groups (n = 13) over a 6-wk treatment period. In comparison to the control group, in the hypothyroid group the relative distribution of type I myosin heavy chain (MHC) was increased 35% (P < 0.05), whereas type IIb MHC decreased 63% (P < 0.05). Similarly, Ca(2+)-activated myosin adenosinetriphosphatase activity (nmol Pi.mg-1.min-1) in the hypothyroid group was reduced 30% compared with the control group (P < 0.05). Furthermore, significant reductions in diaphragmatic maximal tetanic specific tension (Po; N.cm-2; -21%) and maximal shortening velocity (Vmax; muscle length/s; -25%) were observed in the hypothyroid group. These data provide the first evidence that hypothyroid produces a fast-(type IIb) to-slow (type I) shift in costal diaphragmatic MHC isoform profile that is highly correlated to the observed decrease in Vmax. Finally, the present findings indicate that hypothyroidism does not alter myofibrillar content or noncontractile elements of the diaphragm, thereby suggesting an alternative mechanism(s) to explain the reduction in specific Po.
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PMID:Alterations in phenotypic and contractile properties of the rat diaphragm: influence of hypothyroidism. 880 26

In the developing rat cerebrum, the level of different isoforms of Na-K-ATPase mRNA increases significantly during the first three postnatal weeks, which represent the critical period of synaptogenesis and myelination-the two thyroid hormone-sensitive maturational events. To determine the possible functional relationship of these isoforms with maturational events in the developing brain and their mode of regulation by T3, we have examined the effect of hypothyroidism on the expression of the different alpha-isoforms (alpha 1, alpha 2, and alpha 3) of Na-K-ATPase mRNA covering the first 3 wk of postnatal development. Quantitation of these mRNAs from cerebra of 1-, 5-, 10-, 15-, and 20-d-old normal and hypothyroid rats by Northern blot analysis indicate that alpha 3 mRNA is not only predominantly expressed throughout this entire period of study but also represents the species which is most severely affected in the hypothyroid brain. The relative sensitivity for the expression of these mRNAs to T3 were alpha 3 > alpha 1 > alpha 2. These results, together with the report of predominant expression of the alpha 3 isoform in neuronal cells, suggest specific functional involvement of this isoform with the decisive maturational events in the rat brain. Kinetic studies on in vivo induction of Na-K-ATPase alpha-mRNAs by T3 in the 15-d-old hypothyroid rat shows clear stimulation of all the isoforms within 1 h of the administration of the optimal dose (200 micrograms T3/100 g body wt) suggesting a direct, possibly transcriptional effect of the hormone on the expression of these genes.
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PMID:Differential effects of hypothyroidism on Na-K-ATPase mRNA alpha isoforms in the developing rat brain. 890 18

Energy intake profoundly influences many endocrine axes which in turn play a central role in development. The specific influence of a short period of mild hypothyroidism, similar to that induced by undernutrition, in regulating muscle development has been assessed in a large mammal during early postnatal life. Hypothyroidism was induced by providing methimazole and iopanoic acid in the feed of piglets between 4 and 14 d of age, and controls were pair-fed to the energy intake of their hypothyroid littermates. Thyroid status was evaluated, and myofibre differentiation and cation pump concentrations were then assessed in the following functionally distinct muscles: longissimus dorsi (l. dorsi), soleus and rhomboideus. Reductions in plasma concentrations of thyroxine (T4; 32%, P < 0.01), triiodothyronine (T3; 48%, P < 0.001), free T3 (58%, P < 0.001) and hepatic 5'-monodeiodinase (EC 1.11.1.8) activity (74%, P < 0.001) occurred with treatment. Small, although significant, increases in the proportion of type I slow-twitch oxidative fibres occurred with mild hypothyroidism, in l. dorsi (2%, P < 0.01) and soleus (7%, P < 0.01). Nuclear T3-receptor concentration in l. dorsi of hypothyroid animals compared with controls increased by 46% (P < 0.001), a response that may represent a homeostatic mechanism making muscle more sensitive to low levels of circulating thyroid hormones. Nevertheless, Na+, K(+)-ATPase (EC 3.6.1.37) concentration was reduced by 15-16% in all muscles (l. dorsi P < 0.05, soleus P < 0.001, rhomboideus P < 0.05), and Ca(2+)-ATPase (EC 3.6.1.38) concentration was significantly reduced in the two slow-twitch muscles: by 22% in rhomboideus (P < 0.001) and 23% in soleus (P < 0.05). It is concluded that during early postnatal development of large mammals a period of mild hypothyroidism, comparable with that found during undernutrition, induces changes in myofibre differentiation and a down-regulation of cation pumps in skeletal muscle. Such changes would result in slowness of movement and muscle weakness, and also reduce ATP hydrolysis with a concomitant improvement in energetic efficiency.
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PMID:Role of thyroid hormones in early postnatal development of skeletal muscle and its implications for undernutrition. 901 53


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