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Masayoshi Yamaguchi - One of the best experts on this subject based on the ideXlab platform.
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Involvement of nuclear factor-I (NF1) binding motif in the regucalcin gene expression of rat Kidney Cortex: The expression is suppressed by cisplatin administration
Molecular and Cellular Biochemistry, 2001Co-Authors: Hiroyuki Misawa, Masayoshi YamaguchiAbstract:The binding of nuclear factor on the promoter region of the regucalcin gene and the expression of regucalcin in the Kidney Cortex of rats was investigated. Nuclear extracts from Kidney Cortex were used for oligonucleotide competition gel mobility shift assay. An oligonucleotide between position –523 and –506 in the 5′-flanking region of the rat regucalcin gene, which contains a nuclear factor I (NF1) consensus motif TTGGC(N)6CC, competed with the probe for the binding of the nuclear protein from Kidney Cortex. The mutation of TTGGC in the consensus sequence caused an inhibition of the binding of nuclear factors. The binding of nuclear factor on the 5′-flanking region was clearly reduced in the Kidney Cortex obtained at 1, 2, and 3 days after a single intraperitoneal administration of cisplatin (1.0 mg/100 g body wt) to rats. Moreover, cisplatin administration caused a remarkable decrease in regucalcin mRNA levels and regucalcin concentration in the Kidney Cortex. Also, serum regucalcin concentration was significantly decreased by cisplatin administration. Meanwhile, serum urea nitrogen concentration was markedly elevated by cisplatin administration. The present study demonstrates that the specific nuclear factor binds to the NF1-like sequence in the promotor region of regucalcin gene in the Kidney Cortex of rats, and that the nuclear factor binding and regucalcin expression are suppressed by cisplatin administration.
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Stimulatory effect of calcium administration on regucalcin mRNA expression is attenuated in the Kidney Cortex of rats ingested with saline
Molecular and Cellular Biochemistry, 1998Co-Authors: Nobuko Shinya, Masayoshi YamaguchiAbstract:The expression of calcium-binding protein regucalcin mRNA in the Kidney Cortex of rats ingested with saline was investigated. The alteration in regucalcin mRNA levels was analyzed by Northern blotting using liver regucalcin complementary DNA (0.9 kb of open reading frame). Rats were freely given saline as drinking water for 7 days. Regucalcin mRNA levels in the Kidney Cortex were suppressed by saline ingestion. When calcium chloride (10 mg Ca/100 g body weight) was intraperitoneally administered to rats ingested with saline for 7 days, the effect of calcium administration to increase regucalcin mRNA levels was weakened by saline ingestion. Such effect was also seen by the administration of 2.5 and 5 mg Ca/100 g. Regucalcin mRNA levels in the Kidney Cortex of spontaneous hypertensive rats (SHR) were not appreciably increased by the administration of calcium (10 mg/100 g). Meanwhile, calcium content in the Kidney Cortex was significantly elevated by the administration of calcium (10 mg/100 g) to normal rats. This increase was weakened in saline-ingested rats. Moreover, Ca2+/calmodulin-dependent protein kinase activity in the cytosol of Kidney Cortex was significantly decreased by saline ingestion. These results suggest the possibility that saline ingestion-induced suppression of regucalcin mRNA expression in the Kidney Cortex is partly involved in the attenuation of Ca2+ signalling.
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Calcium-binding protein regucalcin mRNA expression in the Kidney Cortex is suppressed by saline ingestion in rats
Molecular and Cellular Biochemistry, 1996Co-Authors: Nobuko Shinya, Hideyuki Kurota, Masayoshi YamaguchiAbstract:The effect of adrenalectomy (ADX) or saline ingestion, which is a hypertensive factor, on the expression of calcium-binding protein regucalcin mRNA in the Kidney Cortex of rats was investigated. The change of regucalcin mRNA levels was analyzed by Northern blotting using rat liver regucalcin complementary DNA (0.9 kb of open-reading frame). Regucalcin mRNA was expressed in the Kidney Cortex but not the medulla. Rats were adrenalectomized, and 48 h later they were sacrificed. ADX caused a reduction of regucalcin mRNA levels in the Kidney Cortex, suggesting that adrenal glands participate in the regulation of the mRNA expression. This reduction was not restored by the subcutaneous administration of dexamethasone with an effective dose (1 mg/kg body weight), which can stimulate Kidney regucalcin mRNA expression. Regucalcin mRNA levels in the Kidney Cortex of rats were markedly suppressed by the ingestion of saline for 7 days. The ADX-induced decrease of renal Cortex regucalcin mRNA levels was not appreciably restored by saline ingestion. Moreover, regucalcin mRNA levels in the Kidney Cortex of spontaneous hypertensive rats (SHR) were clearly decreased as compared with that of control (Wistar-Kyoto) rats. Meanwhile, calcium content in the Kidney Cortex was not significantly decreased by ADX or saline ingestion. The present study suggests that the expression of regucalcin mRNA in the Kidney Cortex of rats is suppressed by saline administration.
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Steroid hormonal regulation of calcium-binding protein regucalcin mRNA expression in the Kidney Cortex of rats
Molecular and Cellular Biochemistry, 1996Co-Authors: Hideyuki Kurota, Masayoshi YamaguchiAbstract:The effect of various steroid hormones on the expression of calcium-binding protein regucalcin mRNA in the Kidney Cortex of rats was investigated. The change of regucalcin mRNA levels was analyzed by Northern blotting using rat liver regucalcin complementary DNA (0.9 kb of open-reading frame). Regucalcin mRNA was expressed in the Kidney Cortex but not the medulla. Rats received a single subcutaneous administration of steroid; the animals were sacrificed 60 min after the treatment of aldosterone (2.5, 5.0 and 10 μg/100 g body weight) or 6 h after the treatment of estrogen (17β-estradiol; 0.05, 0.1 and 0.2 mg/100 g), hydrocortisone (0.5, 1.0 and 3.0 mg/100 g) and dexamethasone (50, 100 and 150 μg/100 g). Regucalcin mRNA levels in the Kidney Cortex were clearly diminished by the administration of aldosterone or estrogen, while hydrocortisone administration had no effect. The administration of dexamethasone (100 μg/100 g) caused a remarkable increase of regucalcin mRNA levels in the Kidney Cortex. The dexamethasone-induced increase in regucalcin mRNA levels was completely blocked by the simultaneous administration of cycloheximide (150 μg/100 g), although the drug administration had no effect on the mRNA levels in control rats. Meanwhile, the dexamethasone administration did not cause an appreciable alteration of calcium content in the Kidney Cortex. The present study demonstrates that, of the various steroid hormones used, dexamethasone uniquely has a stimulatory effect on regucalcin mRNA expression in the Kidney Cortex of rats. The steroid effect may be mediated through a newly synthesized protein.
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expression of calcium binding protein regucalcin mrna in the Kidney Cortex of rats the stimulation by calcium administration
Molecular and Cellular Biochemistry, 1995Co-Authors: Masayoshi Yamaguchi, Hideyuki KurotaAbstract:The expression of calcium-binding protein regucalcin mRNA in the Kidney Cortex of rats was investigated. The change of regucalcin mRNA levels was analyzed by Northern blotting using liver regucalcin complementary DNA (0.9 kb of open-reading frame). Regucalcin mRNA was expressed in the Kidney Cortex, and this expression was clearly increased by a single intraperitoneal administration of calcium chloride solution (5–15 mg Ca/100 g body weight) in rats; this increase was remarkable at 60–120 min after the administration. Thyroparathyroidectomy (TPTX) caused a slight decrease of regucalcin mRNA levels in the Kidney Cortex. However, the administration of calcium (10 mg/100 g) in TPTX rats produced a clear increase of regucalcin mRNA levels in the Kidney Cortex. The subcutaneous administration of calcitonin (10–100 MRC mU/100 g) or parathyroid hormone [1–34] (1–10 U/100 g) in TPTX rats which received calcium (10 mg/100 g) administration did not cause an appreciable alteration of regucalcin mRNA levels in the Kidney Cortex, suggesting that the mRNA expression is not stimulated by calcium-regulating hormones. The administration of trifluoperazine (TFP; 5 mg/100 g), an inhibitor of Ca2+/calmodulin action, completely blocked the expression of regucalcin mRNA stimulated by calcium administration. Now, calcium content in the Kidney Cortex was significantly elevated by a single intraperitpneal administration of calcium (10 mg/100 g) in rats. The present study clearly demonstrates that the expression of regucalcin mRNA in the Kidney Cortex is stimulated by calcium administration in rats. This expression may be mediated through Ca2+/calmodulin action in the Kidney Cortex.
Hideyuki Kurota - One of the best experts on this subject based on the ideXlab platform.
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Calcium-binding protein regucalcin mRNA expression in the Kidney Cortex is suppressed by saline ingestion in rats
Molecular and Cellular Biochemistry, 1996Co-Authors: Nobuko Shinya, Hideyuki Kurota, Masayoshi YamaguchiAbstract:The effect of adrenalectomy (ADX) or saline ingestion, which is a hypertensive factor, on the expression of calcium-binding protein regucalcin mRNA in the Kidney Cortex of rats was investigated. The change of regucalcin mRNA levels was analyzed by Northern blotting using rat liver regucalcin complementary DNA (0.9 kb of open-reading frame). Regucalcin mRNA was expressed in the Kidney Cortex but not the medulla. Rats were adrenalectomized, and 48 h later they were sacrificed. ADX caused a reduction of regucalcin mRNA levels in the Kidney Cortex, suggesting that adrenal glands participate in the regulation of the mRNA expression. This reduction was not restored by the subcutaneous administration of dexamethasone with an effective dose (1 mg/kg body weight), which can stimulate Kidney regucalcin mRNA expression. Regucalcin mRNA levels in the Kidney Cortex of rats were markedly suppressed by the ingestion of saline for 7 days. The ADX-induced decrease of renal Cortex regucalcin mRNA levels was not appreciably restored by saline ingestion. Moreover, regucalcin mRNA levels in the Kidney Cortex of spontaneous hypertensive rats (SHR) were clearly decreased as compared with that of control (Wistar-Kyoto) rats. Meanwhile, calcium content in the Kidney Cortex was not significantly decreased by ADX or saline ingestion. The present study suggests that the expression of regucalcin mRNA in the Kidney Cortex of rats is suppressed by saline administration.
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Steroid hormonal regulation of calcium-binding protein regucalcin mRNA expression in the Kidney Cortex of rats
Molecular and Cellular Biochemistry, 1996Co-Authors: Hideyuki Kurota, Masayoshi YamaguchiAbstract:The effect of various steroid hormones on the expression of calcium-binding protein regucalcin mRNA in the Kidney Cortex of rats was investigated. The change of regucalcin mRNA levels was analyzed by Northern blotting using rat liver regucalcin complementary DNA (0.9 kb of open-reading frame). Regucalcin mRNA was expressed in the Kidney Cortex but not the medulla. Rats received a single subcutaneous administration of steroid; the animals were sacrificed 60 min after the treatment of aldosterone (2.5, 5.0 and 10 μg/100 g body weight) or 6 h after the treatment of estrogen (17β-estradiol; 0.05, 0.1 and 0.2 mg/100 g), hydrocortisone (0.5, 1.0 and 3.0 mg/100 g) and dexamethasone (50, 100 and 150 μg/100 g). Regucalcin mRNA levels in the Kidney Cortex were clearly diminished by the administration of aldosterone or estrogen, while hydrocortisone administration had no effect. The administration of dexamethasone (100 μg/100 g) caused a remarkable increase of regucalcin mRNA levels in the Kidney Cortex. The dexamethasone-induced increase in regucalcin mRNA levels was completely blocked by the simultaneous administration of cycloheximide (150 μg/100 g), although the drug administration had no effect on the mRNA levels in control rats. Meanwhile, the dexamethasone administration did not cause an appreciable alteration of calcium content in the Kidney Cortex. The present study demonstrates that, of the various steroid hormones used, dexamethasone uniquely has a stimulatory effect on regucalcin mRNA expression in the Kidney Cortex of rats. The steroid effect may be mediated through a newly synthesized protein.
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expression of calcium binding protein regucalcin mrna in the Kidney Cortex of rats the stimulation by calcium administration
Molecular and Cellular Biochemistry, 1995Co-Authors: Masayoshi Yamaguchi, Hideyuki KurotaAbstract:The expression of calcium-binding protein regucalcin mRNA in the Kidney Cortex of rats was investigated. The change of regucalcin mRNA levels was analyzed by Northern blotting using liver regucalcin complementary DNA (0.9 kb of open-reading frame). Regucalcin mRNA was expressed in the Kidney Cortex, and this expression was clearly increased by a single intraperitoneal administration of calcium chloride solution (5–15 mg Ca/100 g body weight) in rats; this increase was remarkable at 60–120 min after the administration. Thyroparathyroidectomy (TPTX) caused a slight decrease of regucalcin mRNA levels in the Kidney Cortex. However, the administration of calcium (10 mg/100 g) in TPTX rats produced a clear increase of regucalcin mRNA levels in the Kidney Cortex. The subcutaneous administration of calcitonin (10–100 MRC mU/100 g) or parathyroid hormone [1–34] (1–10 U/100 g) in TPTX rats which received calcium (10 mg/100 g) administration did not cause an appreciable alteration of regucalcin mRNA levels in the Kidney Cortex, suggesting that the mRNA expression is not stimulated by calcium-regulating hormones. The administration of trifluoperazine (TFP; 5 mg/100 g), an inhibitor of Ca2+/calmodulin action, completely blocked the expression of regucalcin mRNA stimulated by calcium administration. Now, calcium content in the Kidney Cortex was significantly elevated by a single intraperitpneal administration of calcium (10 mg/100 g) in rats. The present study clearly demonstrates that the expression of regucalcin mRNA in the Kidney Cortex is stimulated by calcium administration in rats. This expression may be mediated through Ca2+/calmodulin action in the Kidney Cortex.
Shunsuke Furuyama - One of the best experts on this subject based on the ideXlab platform.
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Ribose 1,5-bisphosphate inhibits fructose-1,6-bisphosphatase in rat Kidney Cortex.
Comparative Biochemistry and Physiology B, 2000Co-Authors: Isamu Ozaki, Yuka Mitsui, Hiroshi Sugiya, Shunsuke FuruyamaAbstract:Abstract Fructose-1,6-bisphosphatase is one of the regulatory enzymes of gluconeogenesis in Kidney Cortex. The effect of ribose 1,5-bisphosphate on fructose-1,6-bisphosphatase purified from rat Kidney Cortex was studied. Rat Kidney Cortex, fructose-1,6-bisphosphatase exhibited hyperbolic kinetics with regard to its substrate, but the activity was inhibited by ribose 1,5-bisphosphate at nanomolar concentrations. The inhibitory effect of ribose 1,5-bisphosphate on the fructose-1,6-bisphosphatase was enhanced in the presence of AMP, one of the inhibitors of fructose-1,6-bisphosphatase. Fructose-2,6-bisphosphate, which is an inhibitor of fructose-1,6-bisphosphatase, inhibited rat Kidney Cortex fructose-1,6-bisphosphatase activities at a low concentration of fructose-1,6-bisphosphate but a high concentration of fructose-1,6-bisphosphate relieved fructose-1,6-bisphosphatase from fructose-2,6-bisphosphate-dependent inhibition. On the contrary, fructose-1,6-bisphosphate was not effective for the recovery of fructose-1,6-bisphosphatase from ribose 1,5-bisphosphate-dependent inhibition. These results suggest that ribose 1,5-bisphosphate is a potent inhibitor and is involved in the regulation of fructose-1,6-bisphosphatase in rat Kidney Cortex.
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Ribose 1,5-bisphosphate regulates rat Kidney Cortex phosphofructokinase.
Comparative Biochemistry and Physiology B, 1999Co-Authors: Toyokazu Ozeki, Yuka Mitsui, Hiroshi Sugiya, Shunsuke FuruyamaAbstract:Abstract Phosphofructokinase (EC 2.7.1.11) is a major enzyme of the glycolytic pathway, catalyzing the conversion of fructose 6-phosphate to fructose 1,6-bisphosphate. In this study, we demonstrated the effect of ribose 1,5-bisphosphate on phosphofructokinase purified from rat Kidney Cortex. Ribose 1,5-bisphosphate relieved the phosphofructokinase from ATP inhibition and increased the affinity for fructose 6-phosphate at nanomolar concentrations. These activating effects of ribose 1,5-bisphosphate were enhanced in the presence of AMP. Ribose 1,5-bisphosphate reduced the inhibition of the phosphofructokinase induced by citrate. These results suggest that ribose 1,5-bisphosphate is an activator of rat Kidney Cortex phosphofructokinase and synergistically regulates the enzyme activity with AMP.
Rafael Salto - One of the best experts on this subject based on the ideXlab platform.
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EFFECTS OF STARVATION, DIABETES AND CARBON TETRACHLORIDE INTOXICATION ON RAT Kidney Cortex AND LIVER PYRUVATE CARBOXYLASE LEVELS
Archives of Physiology and Biochemistry, 1996Co-Authors: Rafael Salto, M Sola, F J Oliver, Alberto M. VargasAbstract:Pyruvate carboxylase (PC) has been quantified in rat liver and Kidney Cortex under experimental conditions that modify the gluconeogenic response in both organs: fasting, carbon tetrachloride-induced liver degeneration and alloxan-induced diabetes. Enzymatic activity has been assayed by a 14 CO 2 -fixation method. The amount of enzyme has been determined by competitive ELISA using antibodies raised against the purified rat Kidney Cortex enzyme. Purified fractions of rat-liver and rat-Kidney Cortex PC have been used as standards. Fasting and carbon tetrachloride administration induced a significant increase (25% to 30%) in the amount of enzyme in liver and Kidney Cortex. Alloxan-induced diabetes produced a nearly two-fold increase in the hepatic levels of enzyme without a significant modification in the content of the renal enzyme. These results are discussed on the basis of the different metabolic implications of both organs during the physiological or toxic treatments.
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Citrate inhibition of rat-Kidney Cortex phosphofructokinase
Molecular and Cellular Biochemistry, 1994Co-Authors: María M. Sola, Rafael Salto, F. Javier Oliver, Margarita Gutiérrez, Alberto VargasAbstract:The regulatory properties of citrate on the activity of phosphofructokinase (PFK) purified from rat-Kidney Cortex has been studied. Citrate produces increases in the K_0.5 for Fru-6-P and in the Hill coefficient as well as a decrease in the V_max of the reaction without affecting the kinetic parameters for ATP as substrate. ATP potentiates synergistically the effects of citrate as an inhibitor of the enzyme. Fru-2,6-P_2 and AMP at concentrations equal to K_a were not able to completely prevent citrate inhibition of the enzyme. Physiological concentrations of ATP and citrate produce a strong inhibition of renal PFK suggesting that may participate in the control of glycolysis in vivo .
Alberto Vargas - One of the best experts on this subject based on the ideXlab platform.
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Citrate inhibition of rat-Kidney Cortex phosphofructokinase
Molecular and Cellular Biochemistry, 1994Co-Authors: María M. Sola, Rafael Salto, F. Javier Oliver, Margarita Gutiérrez, Alberto VargasAbstract:The regulatory properties of citrate on the activity of phosphofructokinase (PFK) purified from rat-Kidney Cortex has been studied. Citrate produces increases in the K_0.5 for Fru-6-P and in the Hill coefficient as well as a decrease in the V_max of the reaction without affecting the kinetic parameters for ATP as substrate. ATP potentiates synergistically the effects of citrate as an inhibitor of the enzyme. Fru-2,6-P_2 and AMP at concentrations equal to K_a were not able to completely prevent citrate inhibition of the enzyme. Physiological concentrations of ATP and citrate produce a strong inhibition of renal PFK suggesting that may participate in the control of glycolysis in vivo .
