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)

High affinity (Ca2+ + Mg2+)ATPase activity was demonstrated in proximal tubule basolateral membranes (BLM) obtained from canine kidney. The Km of the enzyme for free Ca2+ was 0.12 +/- 0.02 microM, and at 3 microM free Ca2+, the enzyme reached its maximal velocity. To evaluate hormonal regulation of this enzyme, we studied the in vitro effects of several polypeptide hormones on enzyme activity. We measured the effects of insulin and human (h) PTH-(1-34) and their inactive analogs desoctapeptide insulin, bovine (b) PTH-(3-34), and oxidized hPTH-(1-34); insulin-like growth factors (IGFs) I and II; calcitonin; and the common cellular mediator for PTH and calcitonin, cAMP. At 0.1 microM free Ca2+, insulin (25-100 microU/ml) increased (Ca2+ + Mg2+)ATPase activity in a dose-dependent manner by 35-52% (P less than 0.01) and by 8-13% (P less than 0.05 to P less than 0.01) at a 3-microM free Ca2+ concentration; hPTH-(1-34) PTH (10(-9)-10(-7) M) increased the enzyme activity at a free Ca2+ concentration of 0.1 microM by 13-25% (P less than 0.05 to P less than 0.01). IGF-I increased (Ca2+ + Mg2+)ATPase activity by 40% (P less than 0.05) at 0.1 microM free Ca2+ at high peptide concentrations (10 ng/ml). No effect was obtained at 2 ng/ml IGF-I. cAMP (10(-7)-10(-4) M) stimulated enzyme activity by 18-27% (P less than 0.05 to P less than 0.02) at 0.1 microM Ca2+ and by 8-12% (P less than 0.05 to P less than 0.01) at 3 microM Ca2+. The effects of insulin and cAMP on (Ca2+ + Mg2+)ATPase activity were additive. No effect on the enzyme activity was obtained by the inactive analogs desoctapeptide insulin, bPTH-(3-34), and oxidized hPTH-(1-34), or by calcitonin or IGF-II. The data suggest that insulin and PTH have a specific stimulatory effect on (Ca2+ + Mg2+)ATPase activity in canine kidney proximal tubular BLM. While the insulin action is independent of cAMP, a role of cAMP in the regulatory effect of PTH on this enzyme cannot be ruled out. The direct stimulatory effect of insulin and PTH on (Ca2+ + Mg2+)ATPase in canine kidney proximal tubular BLM suggests that these hormones mediate their cellular effects in part by changes in cellular calcium homeostasis.
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PMID:Hormonal regulation of (Ca2+ + Mg2+)ATPase activity in canine renal basolateral membrane. 302 12

Phosphate (Pi) deprivation and IGFs stimulate renal Pi reabsorption. We studied the involvement of IGFs in the adaptation of Pi transport to Pi deprivation in MDCK cells. Deprivation of Pi for 15 h increased the steady-state content of IGF-II mRNA (77 +/- 12%) whereas IGF-I mRNA was not detectable in MDCK cells in either control or Pi-deprived cells. IGF-II (10(-7) M) and IGF-I (10(-8) M) stimulated the Na-dependent Pi uptake (1.23- and 1.3-fold increase at 15 h respectively). The effect of IGF-I appeared after 15 h and increased up to 40 h of treatment (2.15-fold increase). In contrast, Pi uptake was increased by Pi deprivation as early as 8 h (1.5-fold) and up to 40 h of Pi deprivation (1.9-fold increase). IGF-II mRNA was not increased before 15 h of Pi deprivation and returned to control at 40 h. The combination of IGF-I and Pi deprivation had a more than additive effect on Pi transport (fivefold increase) (P < 0.001). At variance with Pi deprivation, high concentrations of insulin stimulated Na-coupled alanine transport (6 +/- 2% and 16 +/- 4% in Pi-treated and Pi-depleted cells respectively). Pi deprivation and high concentrations of insulin decreased Na,K-ATPase activity (-48 and -64% respectively) and these effects were not additive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Deprivation of phosphate increases IGF-II mRNA in MDCK cells but IGFs are not involved in phosphate transport adaptation to phosphate deprivation. 761 66

Simplex optimization has generated several media that have improved the development of mouse preimplantation embryos in vitro. One objective of this study was to compare the development of preimplantation mouse embryos in one of these computer-optimized media, KSOM, with embryos that developed in vivo, in terms of the relative abundances of specific mRNAs involved in metabolism, transcription, and cell proliferation. First, however, since studies have indicated an improvement of other simple embryo culture media by addition of amino acids, the effects of the addition of amino acids to KSOM (KSOM/AA) on preimplantation development were assessed. We find that addition of both essential and nonessential amino acids to KSOM augments development in vitro, as compared to development supported by KSOM without amino acids. This augmentation is observed starting at the blastocyst stage, and is associated with increased rate of development to the blastocyst stage, increased frequency of hatching, and increased number of cells in the blastocysts. Reverse-transcription PCR was then used to assess the relative abundance of mRNAs for actin, glyceraldehyde-3-phosphate dehydrogenase, Na+, K(+)-ATPase, Sp1, TATA box-binding protein TBP, IGF-I, IGF-II, IGF-I receptor, and IGF-II receptor in embryos that developed in vivo and in vitro using KSOM/AA. Eight out of 9 of these mRNAs were present in the 8-cell embryos and blastocysts raised in KSOM/AA in amounts that were indistinguishable from those in embryos that developed in vivo. It is concluded that KSOM/AA provides an environment in which preimplantation mouse embryos can undergo development that is quantitatively similar to that occurring in vivo.
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PMID:Preimplantation development of mouse embryos in KSOM: augmentation by amino acids and analysis of gene expression. 765 76

GH exerts direct effects on myocardial growth and function. Evidence from laboratory models shows that GH (or IGF-I) induces mRNA expression for specific contractile proteins and myocyte hypertrophy. Furthermore, GH increases the force of contraction and determines myosin phenoconversion toward the low ATPase activity V3 isoform. These data provide plausible explanations for the cardiac abnormalities observed in clinical settings of excessive or defective GH production. In acromegaly, the functional consequences of GH excess initially prevail (hyperkinetic syndrome), followed by alterations of cardiac function when myocardial hypertrophy develops. This involves both ventricles and is purposeless because it occurs without increased wall stress. Hypertrophy also entails proliferation of the myocardial fibrous tissue that leads to interstitial remodeling. The functional consequence is an impaired ventricular relaxation that causes a diastolic dysfunction, followed by impairment of systolic function. In untreated disease, cardiac performance slowly but inexorably deteriorates and heart failure eventually develops. Several lines of evidence support the specificity of heart disease in acromegaly. Particularly demonstrative are the recent studies in which GH production was suppressed by octreotide, with a consequent significant regression of hypertrophy and improvement of cardiac dysfunction. It is not yet established whether full recovery of normal cardiac morphology and function is possible after correction of GH excess. The point is not a minor one since the possibility to revert, albeit partially, myocardial fibrosis is of great relevance to the control of cardiac hypertrophy in general. GHD leads to a reduced mass of both ventricles and to impaired cardiac performance with low heart rate (hypokinetic syndrome). These alterations are particularly evident during physical exercise and might provide an important contribution to the reduced exercise capacity of GHD patients, in addition to the reduced muscle mass and strength. The data also support a role of GH in the maintenance of a normal cardiac structure and performance. The hypokinetic syndrome is well documented in young patients in whom GHD began very early in their childhood. In contrast, the data in adult-onset GHD are less consistent. This suggests that the consequences of GHD are more relevant if the disorder starts during early heart development. As observed with other abnormalities associated with GHD, cardiac dysfunction is also susceptible to marked improvement by hrGH. This observation lends further support to the proposal to treat these patients with replacement therapy.
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PMID:Growth hormone and the heart. 784 68

The effect of ovine GH (oGH) in vivo and recombinant bovine insulin-like growth factor-I (rbIGF-I) in vitro on gill Na+,K(+)-ATPase activity was investigated in two seasonal experiments conducted during the parr-smolt transformation period of coho salmon. In 1991, when fish were held under a photoperiod of 12 h light : 12 h darkness, the stimulatory effect of oGH (1 microgram/g) on gill Na+,K(+)-ATPase in vivo decreased at the time of expected parr-smolt transformation. Gill Na+,K(+)-ATPase from control fish was insensitive to rbIGF-I in vitro from February to June, whereas GH treatment induced sensitivity to rbIGF-I (100-1000 micrograms/l) in vitro in February and March, but not later in development. In 1992, when fish were held under natural conditions, oGH (4 micrograms/g) stimulated gill Na+,K(+)-ATPase in vivo from February to July. There was, however, of pronounced developmental change in sensitivity of gill Na+,K(+)-ATPase to rbIGF-I in vitro. In February, gills from control fish were insensitive, but oGH treatment in vivo induced sensitivity to rbIGF-I in vitro (100-1000 micrograms/l). In April and May, control fish were sensitive to rbIGF-I in vitro. This sensitivity was not further potentiated by oGH treatment in vivo. In June, gills from control or oGH-treated fish were not sensitive to rbIGF-I in vitro, but in July exogenous oGH again induced gill tissue sensitivity to rbIGF-I at 1000 micrograms/l. Both studies showed that rbIGF-I stimulates gill Na(+),K(+)-ATPase directly; an ability that may depend on priming by endogenous or exogenous GH. This supports the role of IGF-I as an endocrine mediator for GH action during parr-smolt transformation.
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PMID:In-vitro effects of insulin-like growth factor-I on gill Na+,K(+)-ATPase in coho salmon, Oncorhynchus kisutch. 785 89

We have previously reported that insulin/insulin-like growth factor (IGF)-I induced the alpha 1 isoform of Na+,K(+)-ATPase in cultured astrocytes. In this study the effects of insulin/IGF-I on Na+,K(+)-ATPase activity and cell proliferation were examined in astrocytes cultured under the various conditions, to test the possible involvement of the enzyme activity in the mitogenic action of IGF-I on astrocytes. Insulin increased Na+,K(+)-ATPase activity and stimulated cell proliferation in subconfluent astrocytes (cultured for 7-14 days in vitro). In contrast, these effects were not observed in confluent cells (cultured for 28 days). Furthermore, insulin stimulated neither the enzyme activity nor [3H]thymidine incorporation in astrocytes preincubated in fetal calf serum-free medium for 2 days (quiescent cells) and treated with dibutyryl cyclic AMP (differentiated cells). The increases in Na+,K(+)-ATPase activity and expression of the alpha 1 mRNA preceded the mitogenic effect. 125I-IGF-I binding experiment showed that all the cells used here had similar binding characteristics. The insulin-induced increase in enzyme activity was not affected by 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), and it was observed even in Ca(2+)-free medium. The stimulation by IGF-I of [3H]thymidine incorporation was attenuated by ouabain and a low external K+ level. These findings suggest that stimulation of Na+,K(+)-ATPase activity is involved in the mitogenic action of IGF-I on cultured astrocytes.
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PMID:Involvement of Na+,K(+)ATPase in the mitogenic effect of insulin-like growth factor-I on cultured rat astrocytes. 859 20

Expression of the Na(+)-K(+)-ATPase alpha-subunit was investigated in the gill and trunk kidney of Salmo trutta. Groups of freshwater (FW) fish were treated with various hormones [cortisol: 3 x 4.0 micrograms/g; recombinant salmon growth hormone (rsGH): 3 x 0.25 micrograms/g; salmon prolactin (sPRL): 3 x 0.25 micrograms/g; recombinant bovine insulin-like growth factor-I (rbIGF-I): 2 x 0.01 micrograms/g; or 2 x 0.1 micrograms/g] or transferred to 25 parts per thousand seawater (SW) and sampled after 1, 2, 3, and 50 days. Total RNA was analyzed by Northern blotting using Xenopus laevis Na(+)-K(+)-ATPase alpha-subunit cDNA as probe. The probe detected a 3.8-kb transcript. Relative to untreated FW control fish, the abundance of alpha-subunit Na(+)-K(+)-ATPase mRNA in gill tissue increased 1.7-to 2.5-fold after treatment with cortisol, rsGH, and rbIGF-I and after transfer to SW. Na(+)-K(+)-ATPase enzyme activity was also significantly stimulated in these groups, except at 0.01 micrograms/g rbIGF-I. sPRL was without effect. In the kidney, alpha-subunit mRNA level and Na(+)-K(+)-ATPase activity were unaffected by hormone treatment and SW transfer. The results indicate that an increased abundance of alpha-subunit mRNA is part of the molecular mechanism behind the increased gill Na(+)-K(+)-ATPase activity induced by SW transfer, cortisol, GH, and IGF-I.
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PMID:Expression of Na(+)-K(+)-ATPase in the brown trout, Salmo trutta: in vivo modulation by hormones and seawater. 859 35

We examined the role of IGF-I in muscle growth stimulated by a beta-adrenergic agonist, clenbuterol. Ewe lambs (90 d old, 20.4 kg mean live weight) were allotted to five groups. A pretreatment control group of five lambs was slaughtered immediately (0 d). The other four groups of six ewes ate freely for 38 or 80 d and were then slaughtered. Half those lambs received clenbuterol (400 micrograms.kg live weight-1.d-1) as a dietary supplement. Blood was collected at intervals from 19 d before supplementation began (0 d) until slaughter. Prerigor muscle samples were sectioned for detection of IGF-I receptors and myofibrillar ATPase activity. Carcass weights were slightly increased by treatment, whereas muscle weights (semimembranosus, gastrocnemius, and biceps femoris) were greatly increased (P < .001), up to 48% at 80 d for semimembranosus. Clenbuterol significantly decreased collagen concentration because myofibrillar proteins were preferentially produced. Collagen solubility was unaffected. Total RNA:total DNA in semimembranosus and gastrocnemius showed transcription was still stimulated between 38 and 80 d. Fiber type area analysis indicated a shift toward glycolytic metabolism, confirmed by iron measurements. However, clenbuterol did not change the portion of muscle occupied by each ATPase class, and the data indicated that type I fibers, though smaller, became relatively more numerous. In spite of significant muscle changes, plasma IGF-I was unaffected by clenbuterol. Similarly, there was no difference in the specific binding of [125I]IGF-I at slaughter between treated and control lambs. However, a response in the first few days of treatment, preceding visible hypertrophy, cannot be excluded.
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PMID:The role of insulin-like growth factor I in clenbuterol-stimulated growth in growing lambs. 861 79

Data is accumulating indicating that impaired insulin action predisposes to increased vascular smooth muscle (VSM) tone, the hallmark of hypertension associated with diabetes. During the last several years, it has been established that VSM is an insulin-sensitive tissue like skeletal muscle and adipocytes. Investigators have shown that insulin regulates VSM intracellular cation metabolism through attenuating effects on inward calcium (Ca2+) currents and by direct effects on VSM cells (VSMCs) Na+, K(+)-ATPase pump expression and activity and that insulin and IGF-I stimulate glucose uptake in VSMCs. Furthermore, recent data suggest that IGF-I, like insulin, attenuates cytosolic calcium [Ca2+]i transients and vasoconstrictive responses. IGF-I, like insulin, also stimulates the production of nitric oxide from both the endothelium and VSMCs. IGF-I and insulin are structurally related, share receptors, and have similar postreceptor actions. Unlike insulin, which must transverse the endothelium before acting on VSMCs in vivo, IGF-I is synthesized by VSMCs. Thus, it is likely that IGF-I has more relevance than insulin in regulating physiological parameters in VSMCs.
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PMID:Effects of insulin and IGF-I on vascular smooth muscle glucose and cation metabolism. 867 90

Skeletal muscles of transgenic mice expressing altered bovine growth hormones (bGH) have been compared with those of nontransgenic mice to determine whether muscle fiber type-specific responses or histopathologies are associated with the altered gene. The slow soleus and predominantly fast gastrocnemius muscles were prepared for myofibrillar ATPase activity (to determine muscle fiber type) and histological examination from mice that were either giant (M4 line), larger than normal (M11 line), dwarf (G119K line), or nontransgenic (NTC). No histopathology was observed in any of the muscles. Although body weights were significantly different between all four lines of mice, only the giant M4 mice had significantly larger muscle fibers than the other lines of mice, while neither the G119K nor M11 lines were significantly different from the NTC for either muscle. No fiber type-specific differences were noted. These results suggest that the different muscles are the product of differences in numbers of muscle fibers expressed in the G119K and M11 lines of mice; the increase in body mass matched the fiber size growth only in the giant M4 line. Therefore, the altered bGH genes may be acting on fetal liver and myoblast/myotube GH receptors to change the GH and IGF-I regulated pattern of muscle development, and eventually, to determine the adult muscle fiber numbers.
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PMID:Effects of bovine growth hormone analogs on mouse skeletal muscle structure. 867 66


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