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PubMed1997

Identification of a new gene product (diphor-1) regulated by dietary phosphate.

Chronic restriction of dietary Pi elicits an increased reabsorption of Pi in the kidney proximal tubules, which involves a stimulation of apical Na-Pi cotransport. This adaptation is in part a direct cellular response of which the mechanism(s) are poorly understood. In this study, the impact of dietary Pi restriction on the differential expression of rat kidney cortex mRNAs was visualized to identify gene products regulated by the Pi status. When kidney cortex mRNAs of rats fed a low- or a high-Pi diet were compared by differential display-polymerase chain reaction (DD-PCR), thirty modulated cDNA bands were observed, of which four were confirmed as being regulated. We focused on one of the upregulated bands, dietary Pi-regulated RNA-1 (diphor-1). A cDNA containing an open reading frame encoding a 52-kDa protein was cloned by library screening. Diphor-1 exhibits a high degree of identity to the Na/H exchanger regulatory factor and to a tyrosine kinase activating protein. Highest expression of diphor-1 mRNA was detected in the kidney (proximal tubules) and in small intestine. Expression experiments showed that diphor-1 specifically increases Na-Pi cotransport in oocytes of Xenopus laevis coinjected with renal type II Na-Pi contransporter cRNA. Further characterizations of diphor-1 will show whether diphor-1 is primarily or secondarily involved in the response to dietary Pi.

Amino Acid Sequence↗
PubMed1983

Inhibition of the alpha-glucosidase specific for collagen disaccharide units in diabetic rat kidney by in vivo glucose levels: possible contribution to basement membrane thickening.

The activity of the alpha-glucosidase specific for collagen disaccharide units has been measured in kidney cortex homogenates of streptozotocin-diabetic rats under three different conditions: (1) in dialyzed homogenates; (2) in non-dialyzed homogenates; (3) in non-dialyzed homogenates to which glucose was added to compensate for dilution due to homogenization and to reach the glucose concentration determined in kidney cortex (37.5 +/- 2.8 mmol/kg diabetic cortex versus 6.8 +/- 0.3 mmol/kg normal cortex). Under the latter condition, the enzyme activity was markedly decreased in diabetic kidney cortex when compared with that of normal age-matched controls: 4.03 +/- 0.25 versus 6.82 +/- 0.29 units/mg protein (p less than 0.001). Inhibition of enzyme activity was also significant in non-dialyzed diabetic homogenates without additional glucose. In the absence of glucose (in the dialyzed homogenates), it is confirmed that the enzyme activity is elevated in diabetic kidney. The glucose inhibition of the enzyme activity has been shown to be important under in vivo conditions. It may therefore contribute to kidney basement membrane thickening.

Animals↗
PubMed1972

Inhibition of cellular transport processes by 5-thio-D-glucopyranose.

5-Thio-d-glucopyranose, the nearest analogue of normal d-glucose, which is proving a useful tool in examinations of d-glucose biochemistry, affects active and facilitated-diffusion transport processes. 5-Thio-d-glucose is readily transported in rabbit kidney-cortex slices and reaches a tissue/medium ratio of 6.5 within 40min. The sulphur analogue shows typical saturation kinetics with a K(m) value of 2.4mm and V(max.) value of 70mumol/h per g of cell water. Uptake of 5-thio-d-glucose is phlorrhizin-sensitive, Na(+)-dependent and energy-dependent. d-Galactose and methyl alpha-d-glucopyranoside transport is competitively inhibited by 5-thio-d-glucose with K(i) values of 4.8 and 9.7mm respectively. 5-Thio-d-glucose thus shows all of the characteristics of active transport in kidney cortex. Transport of neutral amino acids in rat kidney cortex is inhibited by 5-thio-d-glucose. Thus 5.6mm-5-thio-d-glucose causes a 25-30% inhibition of the transport of glycine and the non-metabolized amino acids cycloleucine and alpha-aminoisobutyric acid. 5-Thio-d-glucose is freely taken up by the facilitated-diffusion transport system in rat diaphragm muscle. The sulphur analogue inhibits the transport of d-xylose in this tissue but has no effect on the uptake of d-arabinose. It is concluded that the ring heteroatom is not an effector of binding in the transport processes examined and causes no important alteration in the conformation of the sugar. The diabetogenic action produced by 5-thio-d-glucose is due, in part, to the ability of the analogue to interfere with cellular transport processes that use d-glucose.

Amino Acids↗
PubMed1999

Clinical significance of nm23 expression in renal cell carcinoma.

In many tumors an expression of nm23 gene products is associated with a lower metastatic potential. The aim was to evaluate whether nm23 gene expression in renal cell carcinoma was associated with clinicopathological findings and survival. In 41 patients, the expression of nm23 protein was analyzed in tumor and corresponding kidney cortex tissue by immunohistochemical analysis using a monoclonal nm23-H1 antibody. In all kidney cortex samples intense nm23 staining was found. Of 41 tumors, 15 had high, 12 intermediate, 5 low nm23 expression whereas 9 tumors showed none. There were no differences in nm23 staining between different stages, grades or size of tumor. No correlation between survival and nm23 expression was observed. However, diploid tumors had significantly less nm23 staining compared with aneuploid tumors, indicating that nm23 gene inactivation might be a favorable sign. The expression of nm23 gene products seems not to be correlated to tumor progression and metastatic ability in renal cell carcinoma.

Adult↗
PubMed1979

Prolyl 3-hydroxylase and 4-hydroxylase activities in certain rat and chick-embryo tissues and age-related changes in their activities in the rat.

Prolyl 3-hydroxylase activity, expressed per unit of extract protein, was much higher in rat kidney cortex than in the lung, liver or skin. A marked decrease in activity was found in the kidney cortex, liver and skin beyond 10 days of age. The ratio of prolyl 3-hydroxylase to 4-hydroxylase activity in the kidney cortex was 13--17 times that in the skin, that in the liver 6--8 times, and that in the lung about twice the value for the skin, there being no changes in this ratio with age. In 16-day chick embryos the highest ratios of prolyl 3-hydroxylase to 4-hydroxylase activity were found in the liver, heart, lens, aorta and kidney, and the lowest ratios in tendon, cartilage, cartilaginous and membranous bone and skin. The results suggest that the differences in the extent of prolyl 3-hydroxylation between various collagens can in part be explained by differences in the amount of prolyl e-hydroxylase activity among different cells.

Aging↗
PubMed1984

Age dependence of the gamma-carboxyglutamic acid containing proteins.

A distinct age dependence was observed in the occurrence of the gamma-carboxyglutamic acid containing proteins obtained from kidney cortex, liver and femoral bone. In the femoral bone, a stepped increase was seen when comparing animals 60, 350 and 700 days old. In the liver and mainly in the kidney cortex there was no change during the first year of life, but a distinct increase in the gamma-carboxyglutamate containing proteins was seen between day 350 and 700. It was also established that the increased level of gamma-carboxyglutamate at least in kidney cortex is due to a more intense carboxylation reaction in older animals as increased incorporation of labelled bicarbonate was observed in the microsomal fraction. In accordance with our previous results the occurrence of the carboxyglutamic acid containing proteins was shown to be vitamin D dependent; in vitamin D deprived animals supplemented with this vitamin the reappearance of gamma-carboxylate is more distinct in situations where higher levels of gamma-carboxyglutamic acid occur physiologically.

1-Carboxyglutamic Acid↗
PubMed1995

Dexamethasone inhibits inorganic phosphate stimulated Ca(2+)-dependent damage of isolated rat liver and renal cortex mitochondria.

The prevention of Ca(2+)-induced permeabilization of rat liver and kidney cortex mitochondria by dexamethasone, a common anti-inflammatory glucocorticoid, was the subject of this study. A non-specific release of matrix Ca2+ and membrane depolarization was observed in respiring mitochondrial suspensions subjected to a 30 nmol Ca2+/mg protein load in the presence of 2 mM inorganic phosphate (Pi), or 20 nmol Ca2+/mg protein with 1 mM Pi, for liver and renal cortex mitochondria (RCM), respectively. Additions of dexamethasone prior to Ca2+ in mitochondrial suspensions from liver or kidney cortex (80 and 200 microM final concentrations, respectively) led to 75-80% protection from these permeabilization-associated alterations of functional integrity. In conclusion, dexamethasone appears to show great promise in blocking the opening of a Ca(2+)-dependent 'non-specific pore' in the inner membranes of mitochondria from various sources.

Animals↗
PubMed1987

Orientation of vesicles isolated from baso-lateral membranes of renal cortex.

Baso-lateral membranes were isolated from the canine and porcine kidney cortex by several different methods currently in use. Sidedness of the isolated membrane vesicles was determined by procedures using 1. ouabain-sensitive (Na+K+)ATPase assays in the presence and in the absence of sodium dodecylsulfate or digitoxigenin plus monensin, 2. (Na+, K+, Mg2+)ATPase assays with valinomycin, 3. sialidase accessibility, and 4. binding of hydrophilic and lipophilic cardiac glycosides. The (Na+K+)ATPase activity in the membrane preparation was increased 10-fold of that found in the crude homogenate. Isolated membrane vesicles, prepared by different techniques, were all found to be overwhelmingly of right-side-out orientation;namely, right-side-out = 51-68%, inside-out = 4-13%, and unsealed vesicles = 26-42%. Results of sidedness determinations by different methods showed a good agreement. Thus, predominantly right-side-out oriented vesicles are formed during conventional isolation procedures for membranes of the kidney cortex.

Animals↗
PubMed2005

Duration of streptozotocin-induced diabetes differentially affects p38-mitogen-activated protein kinase (MAPK) phosphorylation in renal and vascular dysfunction.

BACKGROUND: In the present study we tested the hypothesis that progression of streptozotocin (STZ)-induced diabetes (14-days to 28-days) would produce renal and vascular dysfunction that correlate with altered p38- mitogen-activated protein kinase (p38-MAPK) phosphorylation in kidneys and thoracic aorta. METHODS: Male Sprague Dawley rats (350-400 g) were randomized into three groups: sham (N = 6), 14-days diabetic (N = 6) and 28-days diabetic rats (N = 6). Diabetes was induced using a single tail vein injection of STZ (60 mg/kg, I.V.) on the first day. Rats were monitored for 28 days and food, water intake and plasma glucose levels were noted. At both 14-days and 28-days post diabetes blood samples were collected and kidney cortex, medulla and aorta were harvested from each rat. RESULTS: The diabetic rats lost body weight at both 14-days (-10%) and 28-days (-13%) more significantly as compared to sham (+10%) group. Glucose levels were significantly elevated in the diabetic rats at both 14-days and 28-days post-STZ administration. Renal dysfunction as evidenced by renal hypertrophy, increased plasma creatinine concentration and reduced renal blood flow was observed in 14-days and 28-days diabetes. Vascular dysfunction as evidenced by decreased carotid blood flow was observed in 14-days and 28-days diabetes. We observed an up-regulation of inducible nitric oxide synthase (iNOS), prepro endothelin-1 (preproET-1) and phosphorylated p38-MAPK in thoracic aorta and kidney cortex but not in kidney medulla in 28-days diabetes group. CONCLUSION: The study provides evidence that diabetes produces vascular and renal dysfunction with a profound effect on signaling mechanisms at later stage of diabetes.

Animals↗
PubMed1985

Effects of deficient and adequate dietary magnesium concentrations on body magnesium concentrations in wethers.

Effects of 2 dietary Mg concentrations (deficient and adequate: 0.04 and 0.12 g of Mg/100 g of dry matter, respectively) on body fluid and tissue Mg concentrations and performance of wether lambs were evaluated in a 28-day trial. Nine blood and 6 urine samples were collected from each wether. After 28 days, CSF and wool samples were collected, and diet, body fluids, and tissues were analyzed for mineral concentration. Diet effects on serum and urine Mg concentrations were noticed after day 3 (P less than 0.01; P less than 0.05, respectively). Mean serum and urine Mg concentrations for 6 sampling periods were correlated (r = 0.83, P less than 0.001; No. of samples = 12). The effect of dietary Mg on CSF Mg concentrations approached significance (P less than 0.10). Effects of diet on cardiac muscle, liver, and 3rd metatarsal bone Mg contents or hematologic criteria were not observed. Diet affected wool and kidney cortex Mg contents (P less than 0.02). Individual mean 28-day serum Mg concentration was correlated with wool Mg content (r = 0.73, P less than 0.05; n = 8) and with kidney cortex Mg content (r = 0.75, P less than 0.05; n = 8). Wethers fed low Mg diet excreted less urine Ca (P less than 0.001) and had slightly lower serum Ca and K values (P less than 0.10) than did wethers fed high Mg. Significant differences in cardiac muscle, liver, spleen, or kidney cortex Ca contents were not observed. Wethers fed low Mg diet consumed less dry matter and gained less weight (P less than 0.001) than did wethers fed high Mg diet. Body fluid and tissue macromineral concentrations of 1 wether with hypomagnesemic tetany are presented for prognostic and diagnostic purposes.

Animals↗
PubMed2004

Upregulation of macula densa cyclooxygenase-2 expression is not dependent on glomerular filtration.

Although the regulation of cyclooxygenase-2 (COX-2) expression in the kidney cortex has been extensively characterized, the physiological control mechanisms of COX-2 expression at the level of the kidney and at the level of the tubular cells are not well understood. Based on the current hypothesis that tubular salt transport might be a crucial regulator of COX-2 expression, this study aimed to determine the impact of salt delivery to the tubules (glomerular filtration) for the regulation of COX-2 in the kidney cortex in vivo. To this end, glomerular filtration of the right kidney was abrogated by the ligation of the right ureter of male Sprague-Dawley rats. After 1 wk of ligation, the animals were treated with subcutaneous infusions of furosemide (12 mg x kg(-1) x day(-1)) or with a low-salt or a high-salt diet (0.02% wt/wt; 8% wt/wt), and COX-2 as well as renin mRNA expression were determined in the ligated and the nonligated contralateral kidney. During ureteral ligation, hydronephrosis developed with a reduction of medullary mass, while the cortex was preserved. Expressions of the Na-K-2Cl cotransporter isoforms A and B were both reduced in the hydronephrotic cortex to 70 and 35% of the corresponding contralateral intact kidney. Despite the abrogation of glomerular filtration, detected by inulin clearance measurements, renocortical COX-2 mRNA abundance was stimulated by furosemide treatment (3.2-fold) or low-salt diet (2.9-fold) to similar degrees compared with the intact contralateral kidney (2.7-fold for both treatments), whereas a high-salt diet did not significantly suppress COX-2 mRNA in the macula densa region of either kidney. Renin mRNA expression was regulated strictly in parallel in both kidneys, a low-salt diet or furosemide treatment stimulating and a high-salt diet suppressing it. We conclude from these findings that salt delivery to the tubules is not an essential requirement for the upregulation of COX-2 by salt deficiency or by loop diuretics in the rat kidney cortex nor is it for chronic stimulation of renin mRNA expression.

Animals↗
PubMed1984

Reduced cadmium body burden in cadmium-exposed calves fed supplemental zinc.

The objectives of this study were to evaluate the use of practical supplemental dietary zinc to modify the cadmium content in edible bovine tissues and to identify copper interactions with cadmium and zinc. The effect of supplemental zinc (200 or 600 micrograms/g) on the concentrations of cadmium, zinc, and copper in liver, kidney cortex, muscle, and blood of calves fed 50 micrograms/g cadmium for 60 days was evaluated. Blood samples were collected before and eight times after starting to feed cadmium or cadmium plus zinc. Liver, kidney, and muscle samples were collected when calves were slaughtered (baseline, at beginning of experimental feeding; cadmium-fed, at end of 60 days feeding). The cadmium concentrations of all sample types collected were markedly increased by the feeding of cadmium. Feeding 600 micrograms/g supplemental zinc significantly increased the zinc concentrations of liver, kidney cortex, and blood and decreased the cadmium accumulation in these organs as well as muscle. The copper concentrations of muscle or blood were not altered by feeding cadmium with or without zinc but those of liver and kidney cortex were significantly increased by higher dietary levels of zinc and cadmium. The potential use of dietary zinc salts in reducing cadmium body burden in food animals suspected or known to have high cadmium intakes is suggested.

Animals↗
PubMed2002

Interaction with grp58 increases activity of the thiazide-sensitive Na-Cl cotransporter.

The thiazide-sensitive sodium-chloride cotransporter (NCC) is expressed by distal convoluted tubule cells of the mammalian kidney. We used yeast two-hybrid screening to identify that glucose-regulated protein 58 (grp58), a protein induced by glucose deprivation, binds to the COOH terminus of the NCC. Immunoprecipitation of rat kidney cortex homogenates using a guinea pig anti-NCC antibody confirmed that grp58 associates with the NCC in vivo. Northern blots indicated that grp58 is highly expressed in rat kidney cortex. Immunofluorescence showed that grp58 protein abundance in kidney is highest in epithelial cells of the distal nephron, where it colocalizes with NCC near the apical membrane. To determine whether this interaction has a functional significance, NCC and grp58 cRNA were coexpressed in Xenopus laevis oocytes. In oocytes overexpressing grp58, sodium uptake was increased compared with control. Because oocytes express endogenous grp58, antisense experiments were performed to evaluate whether endogenous grp58 affected NCC activity in oocytes. Sodium uptake was lower in oocytes injected with both antisense grp58 cRNA and sense NCC compared with sense NCC oocytes. Western blot analysis did not show any effect of grp58 expression on processing of the NCC. These data indicate a novel, functionally important interaction between grp58 and the NCC in rat kidney cortex.

Animals↗
PubMed1986

Effect of peroxisomal proliferators on microsomal prostaglandin A omega-hydroxylase.

Earlier, we reported the isolation of a cytochrome P-450 highly active in prostaglandin A (PGA) omega-hydroxylation (PGA omega-hydroxylase) from rabbit kidney cortex, small intestine, and colon microsomes. In the present studies, the effects of peroxisomal proliferating agents on the PGA omega-hydroxylase have been examined. Administration of clofibrate or di(2-ethylhexyl)phthalate (DEHP) resulted in a significant increase in the PGA1 omega-hydroxylase activity of kidney cortex, liver, and small intestine microsomes. Similar findings were also obtained for laurate hydroxylase activity in kidney and liver microsomes. Kidney PGA omega-hydroxylase (designated cytochrome P-450ka) was isolated and highly purified from clofibrate- or DEHP-treated rabbits, with a yield 3 times higher than that from untreated, or phenobarbital- or 3-methylcholanthrene-treated rabbits. Cytochrome P-450ka from clofibrate- or DEHP-treated rabbits exhibited the same properties as those from untreated rabbits. Guinea pig antiserum against cytochrome P-450ka strongly inhibited the omega-hydroxylation of PGA1 by kidney cortex microsomes from clofibrate-treated rabbits. The PGA1 omega-hydroxylase activity of clofibrate-treated liver microsomes was also inhibited by this antiserum, suggesting that a PGA omega-hydroxylase immunochemically related to cytochrome P-450ka exists in liver microsomes.

Animals↗
PubMed2004

ErbB4 is downregulated in renal cell carcinoma--a quantitative RT-PCR and immunohistochemical analysis of the epidermal growth factor receptor family.

In the present study the authors evaluated the expression of the EGFR family members ErbB2-4 in renal cell carcinoma (RCC). Thirty-one RCCs were examined for gene expression of ErbB2-4 mRNA by quantitative real-time RT-PCR. For eight of the patients samples of nonneoplastic kidney cortex were also evaluated. Expression of ErbB4 mRNA was analysed in the eight matched tumour and kidney cortex samples by isoform-specific real-time RT-PCR analysis. ErbB4 protein expression was analysed by immunohistochemistry. In summary the results showed that ErbB2 mRNA was downregulated in conventional (clear cell) RCC; ErbB3 mRNA levels were low and heterogeneous in both tumours and kidney cortex; ErbB4 mRNA and protein were strongly downregulated in conventional and papillary RCC. Thus, ErbB2 and ErbB4 are not likely to be oncogenes in the majority of RCCs; instead, the observed downregulations suggest that these receptors might function as tumour suppressors in RCC.

Adult↗
PubMed1993

Identification of two unique polypeptides from dog kidney outer cortex and outer medulla that exhibit different Na+/D-glucose cotransport functional properties.

The cloned Na+/D-glucose cotransporter SGLT1 and an additional recently isolated human kidney cDNA Hu14/K15 belong to a family of similar cotransport proteins including the Na(+)-dependent nucleoside and Na(+)-dependent myo-inositol carrier SMIT1. For the present study we used two different polyclonal antibodies raised against the amino acid sequence 402-420 (Ab-E) and 565-574 (Ab-P) of SGLT1 to probe brush-border membrane fractions from different regions (outer cortex-->outer medulla) of dog kidney. In Western blots both Ab-E and Ab-P react specifically (peptide blockable) with two distinct bands migrating on SDS-PAGE under reducing conditions at 75.5 kDa and 72.5 kDa. The higher molecular mass polypeptide is greatly enriched (13:1) in outer cortex and diminishes progressively towards outer medulla, whereas the lower molecular mass band is barely detectable in outer cortex but is enriched in outer medulla (4:1). Brush-border membrane vesicles (BBMV) prepared from the same outer cortical and outer medullary regions that were probed with Ab-E and Ab-P exhibit strikingly different Na+/D-glucose functional transport behavior. The Na+/D-glucose cotransport activity in outer cortical BBMV is a low-affinity system with Km = 5.98 +/- 1.01 mM, Vmax = 13.05 +/- 0.55 nmol/mg protein per min, and with 1:1 Na+:D-glucose stoichiometry. Outer medulla BBMV exhibit high-affinity Km = 0.27 +/- 0.03 mM Vmax = 0.97 +/- 0.04 nmol/mg protein per min and 2:1 Na+:D-glucose stoichiometry. Comparison of SGLT1, Hu14/K15, SNST1 and SMIT indicates that Ab-E could cross react with all four, but Ab-P would recognize SGLT1, Hu14/K15, SNST1 but not SMIT. Also SNST1 is not expressed in outer cortex. Based on currently available sequence data, and its marked enrichment in outer cortex, the 75.5 kDa band is a likely candidate protein responsible for low-affinity and 1:1 Na+:D-glucose stoichiometric Na+/D-glucose cotransport activity (Hu14/K15) while the minor 72.5 kDa band in outer cortex is probably SGLT1. In outer medulla, the predominant band recognized by both Ab-E and Ab-P is the 72.5 kDa protein and this could be either SGLT1 or SNST1.

Antibodies↗
PubMedDate not supplied

Study of correlation of Se content in human hair and internal organs by INAA.

The correlations of essential element Se between human hair and kidney-cortex, liver, and lung from the same subjects were investigated by instrumental neutron activation analysis, using the reaction 76Se (n, gamma) 77mSe, for 24 Chinese autopsies. The concentration of Se is higher in kidney-cortex (2.04-5.36 mg/kg) than in liver (0.73-2.29), lung (0.50-1.85), and hair (0.37-1.43). It is important to know that there are significant relationships of Se concentration between hair and the other three internal organs. The correlation coefficient by linear regression analysis are 0.639, 0.570, and 0.635 for liver, lung, and kidney-cortex, respectively; and the P values are all less than 0.01 for the three tissues.

Adult↗
PubMed1986

Decreased Na+-K+-ATPase activity and [3H]ouabain binding sites in various tissues of spontaneously hypertensive rats.

Na+-K+-ATPase activity and [3H]ouabain binding were studied in cerebral cortex, kidney and heart isolated from spontaneously hypertensive rats (SHR) in both the prehypertensive (6 week old) and the hypertensive stages (14 week old). Na+-K+-ATPase activity of heart and kidney was found to be decreased by about 38 and 16% in the prehypertensive and hypertensive stages of SHR respectively; that of cerebral cortex decreased by 23.5% only in the hypertensive stages. Similar results were obtained by pretreatment of membranes with either 0.001% Triton X-100 or by increasing the K concentration from 4.7 to 12.7 mM in the Krebs solution. No significant differences in microsomal protein yield were noted between prehypertensive or hypertensive SHR and the age-matched WKY rats. The study of binding of [3H]ouabain to cerebral cortex, kidney and heart showed that the decreased Na+-K+-ATPase in hypertensive SHR was due to a 31.6, 21.8 and 41.3% reduction in the number of high affinity binding sites respectively, while the affinity constants (Kd) of ouabain binding sites on this enzyme in cerebral cortex, kidney and heart of the normotensive WKY rats were 26.5, 455.9 and 74.7 nM respectively and those from the hypertensive SHR were not altered. The plasma K concentration of the SHR in the prehypertensive and hypertensive stages was 4.07 and 4.13 mM, respectively, significantly less than that of the age-matched WKY rats. It appears that the decrease of plasma K and Na+-K+-ATPase activity in heart and kidney in SHR is derived from a genetic defect and may be related to the abnormal Na handling in this genetically hypertensive strain.

Animals↗