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Article ; Online: Dopamine reduces cell surface Na

Hu, Ming Chang / Bobulescu, I Alexandru / Quiñones, Henry / Gisler, Serge M / Moe, Orson W

American journal of physiology. Renal physiology

2017 Volume 313, Issue 4, Page(s) F1018–F1025

Abstract: The intrarenal autocrine-paracrine dopamine (DA) system mediates a significant fraction of the natriuresis in response to a salt load. DA inhibits a number of ... ...

Abstract	The intrarenal autocrine-paracrine dopamine (DA) system mediates a significant fraction of the natriuresis in response to a salt load. DA inhibits a number of Na
MeSH term(s)	Animals ; Cell Membrane/drug effects ; Cell Membrane/metabolism ; Cells, Cultured ; Didelphis ; Dopamine/pharmacology ; Dose-Response Relationship, Drug ; Down-Regulation ; Exocytosis/drug effects ; Kidney/drug effects ; Kidney/metabolism ; Natriuresis/drug effects ; Protein Transport ; Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers/metabolism ; Time Factors
Chemical Substances	Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2017-08-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00251.2017
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Article ; Online: Luminal Na(+)/H (+) exchange in the proximal tubule.

Bobulescu, I Alexandru / Moe, Orson W

Pflugers Archiv : European journal of physiology

2008 Volume 458, Issue 1, Page(s) 5–21

Abstract: The proximal tubule is critical for whole-organism volume and acid-base homeostasis by reabsorbing filtered water, NaCl, bicarbonate, and citrate, as well as by excreting acid in the form of hydrogen and ammonium ions and producing new bicarbonate in the ...

Abstract	The proximal tubule is critical for whole-organism volume and acid-base homeostasis by reabsorbing filtered water, NaCl, bicarbonate, and citrate, as well as by excreting acid in the form of hydrogen and ammonium ions and producing new bicarbonate in the process. Filtered organic solutes such as amino acids, oligopeptides, and proteins are also retrieved by the proximal tubule. Luminal membrane Na(+)/H(+) exchangers either directly mediate or indirectly contribute to each of these processes. Na(+)/H(+) exchangers are a family of secondary active transporters with diverse tissue and subcellular distributions. Two isoforms, NHE3 and NHE8, are expressed at the luminal membrane of the proximal tubule. NHE3 is the prevalent isoform in adults, is the most extensively studied, and is tightly regulated by a large number of agonists and physiological conditions acting via partially defined molecular mechanisms. Comparatively little is known about NHE8, which is highly expressed at the lumen of the neonatal proximal tubule and is mostly intracellular in adults. This article discusses the physiology of proximal Na(+)/H(+) exchange, the multiple mechanisms of NHE3 regulation, and the reciprocal relationship between NHE3 and NHE8 at the lumen of the proximal tubule.
MeSH term(s)	Acid-Base Equilibrium/physiology ; Adult ; Gene Expression Regulation ; Humans ; Infant, Newborn ; Kidney Tubules, Proximal/metabolism ; Protein Isoforms/metabolism ; Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers/agonists ; Sodium-Hydrogen Exchangers/physiology
Chemical Substances	Protein Isoforms ; SLC9A3 protein, human ; SLC9A8 protein, human ; Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers
Language	English
Publishing date	2008-10-14
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-008-0595-1
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Article: Na+/H+ exchangers in renal regulation of acid-base balance.

Bobulescu, I Alexandru / Moe, Orson W

Seminars in nephrology

2006 Volume 26, Issue 5, Page(s) 334–344

Abstract: The kidney plays key roles in extracellular fluid pH homeostasis by reclaiming bicarbonate (HCO(3)(-)) filtered at the glomerulus and generating the consumed HCO(3)(-) by secreting protons (H(+)) into the urine (renal acidification). Sodium-proton ... ...

Abstract	The kidney plays key roles in extracellular fluid pH homeostasis by reclaiming bicarbonate (HCO(3)(-)) filtered at the glomerulus and generating the consumed HCO(3)(-) by secreting protons (H(+)) into the urine (renal acidification). Sodium-proton exchangers (NHEs) are ubiquitous transmembrane proteins mediating the countertransport of Na(+) and H(+) across lipid bilayers. In mammals, NHEs participate in the regulation of cell pH, volume, and intracellular sodium concentration, as well as in transepithelial ion transport. Five of the 10 isoforms (NHE1-4 and NHE8) are expressed at the plasma membrane of renal epithelial cells. The best-studied isoform for acid-base homeostasis is NHE3, which mediates both HCO(3)(-) absorption and H(+) excretion in the renal tubule. This article reviews some important aspects of NHEs in the kidney, with special emphasis on the role of renal NHE3 in the maintenance of acid-base balance.
MeSH term(s)	Acid-Base Equilibrium/physiology ; Acidosis/physiopathology ; Adaptation, Physiological ; Animals ; Humans ; Nephrons/physiology ; Sodium-Hydrogen Exchangers/physiology
Chemical Substances	Sodium-Hydrogen Exchangers
Language	English
Publishing date	2006-11-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604652-6
ISSN	1558-4488 ; 0270-9295
ISSN (online)	1558-4488
ISSN	0270-9295
DOI	10.1016/j.semnephrol.2006.07.001
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Article ; Online: Net Acid Excretion and Urinary Organic Anions in Idiopathic Uric Acid Nephrolithiasis.

Bobulescu, I Alexandru / Park, Sun K / Xu, L H Richie / Blanco, Francisco / Poindexter, John / Adams-Huet, Beverley / Davidson, Taylor L / Sakhaee, Khashayar / Maalouf, Naim M / Moe, Orson W

Clinical journal of the American Society of Nephrology : CJASN

2019 Volume 14, Issue 3, Page(s) 411–420

Abstract: Background and objectives: Idiopathic uric acid nephrolithiasis, which is closely associated with obesity and the metabolic syndrome, is increasing in prevalence. Unduly acidic urine pH, the quintessential pathophysiologic feature of this disease, is in ...

Abstract	Background and objectives: Idiopathic uric acid nephrolithiasis, which is closely associated with obesity and the metabolic syndrome, is increasing in prevalence. Unduly acidic urine pH, the quintessential pathophysiologic feature of this disease, is in part explained by inadequate excretion of the principal urinary buffer ammonium. The role of net acid excretion in the pathogenesis of uric acid nephrolithiasis is incompletely understood. Design, setting, participants, & measurements: We compared acid-base parameters of patients with idiopathic uric acid nephrolithiasis with matched control subjects under controlled diets in an inpatient metabolic unit. Measurements included fasting blood and 24-hour urine chemistries and 24-hour urine metabolomic analysis. Comparisons between groups included analysis of covariance models controlling for urine pH or body mass index. Results: Subjects with idiopathic uric acid nephrolithiasis had lower urine pH (5.5 versus 5.9; Conclusions: Higher acid load to the kidney, resulting in higher urinary net acid excretion, is an important factor in the pathogenesis of idiopathic uric acid nephrolithiasis.
MeSH term(s)	Acid-Base Equilibrium ; Biomarkers/urine ; Body Mass Index ; Case-Control Studies ; Diet/adverse effects ; Female ; Humans ; Hydrogen-Ion Concentration ; Kidney/physiopathology ; Male ; Middle Aged ; Nephrolithiasis/diagnosis ; Nephrolithiasis/etiology ; Nephrolithiasis/physiopathology ; Nephrolithiasis/urine ; Pilot Projects ; Renal Elimination ; Risk Factors ; Uric Acid/urine
Chemical Substances	Biomarkers ; Uric Acid (268B43MJ25)
Language	English
Publishing date	2019-02-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2226665-3
ISSN	1555-905X ; 1555-9041
ISSN (online)	1555-905X
ISSN	1555-9041
DOI	10.2215/CJN.10420818
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Article ; Online: Quantification of renal steatosis in type II diabetes mellitus using dixon-based MRI.

Yokoo, Takeshi / Clark, Haley R / Pedrosa, Ivan / Yuan, Qing / Dimitrov, Ivan / Zhang, Yue / Lingvay, Ildiko / Beg, Muhammad S / Bobulescu, I Alexandru

Journal of magnetic resonance imaging : JMRI

2016 Volume 44, Issue 5, Page(s) 1312–1319

Abstract: Purpose: To evaluate renal lipid content in subjects with and without type II diabetes mellitus (DM2) using Dixon-based magnetic resonance imaging (MRI).: Materials and methods: This retrospective study was approved by the Institutional Review Board ... ...

Abstract	Purpose: To evaluate renal lipid content in subjects with and without type II diabetes mellitus (DM2) using Dixon-based magnetic resonance imaging (MRI). Materials and methods: This retrospective study was approved by the Institutional Review Board and compliant with the Health Insurance Portability and Accountability Act. Sixty-nine adults with or without DM2 (n = 29, n = 40) underwent 3T MRI of the abdomen using 3D multiecho Dixon gradient-echo acquisition and proton-density fat fraction (FF) reconstruction. FF values were recorded within segmented regions of interest in the kidneys and liver. The FF measurement error was estimated from the within-subject difference between the right and left kidneys using Bland-Altman analysis. Correlation between renal FF, hepatic FF, and body mass index (BMI) was evaluated. The association between renal FF and DM2 was evaluated by Wilcoxon rank sum test as well as by multivariate regression to correct for potential confounding effects of age, sex, BMI, creatinine, and hepatic FF. P < 0.05 was considered statistically significant. Results: Per-subject 95% limits of agreement of the renal FF measurement were [-3.26%, +3.22%]. BMI was significantly correlated with renal FF (r = 0.266, P = 0.027) and with liver FF (r = 0.344, P = 0.006). Correlation between renal and hepatic FF did not reach statistical significance (r = 0.215, P = 0.090). Median renal FF (±interquartile range) was 2.18% (±2.52%) in the DM2 cohort, significantly higher than 0.80% (±2.63%) in the non-DM2 cohort (P < 0.001). After correcting for potential confounders, the relationship between DM2 and renal FF remained statistically significant (P = 0.005). Conclusion: Renal lipid content can be measured noninvasively using Dixon-based MRI and may be increased in subjects with DM2 compared to those without DM2. J. Magn. Reson. Imaging 2016;44:1312-1319.
MeSH term(s)	Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/diagnostic imaging ; Diabetes Mellitus, Type 2/metabolism ; Diabetic Nephropathies/diagnostic imaging ; Diabetic Nephropathies/etiology ; Diabetic Nephropathies/metabolism ; Female ; Humans ; Image Enhancement/methods ; Image Interpretation, Computer-Assisted/methods ; Lipid Metabolism ; Magnetic Resonance Imaging/methods ; Male ; Middle Aged ; Molecular Imaging/methods ; Reproducibility of Results ; Sensitivity and Specificity
Language	English
Publishing date	2016-03-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1146614-5
ISSN	1522-2586 ; 1053-1807
ISSN (online)	1522-2586
ISSN	1053-1807
DOI	10.1002/jmri.25252
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Zs.A 3648: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Adiponectin alters renal calcium and phosphate excretion through regulation of klotho expression.

Rutkowski, Joseph M / Pastor, Johanne / Sun, Kai / Park, Sun K / Bobulescu, I Alexandru / Chen, Christopher T / Moe, Orson W / Scherer, Philipp E

Kidney international

2016 Volume 91, Issue 2, Page(s) 324–337

Abstract: The kidney controls systemic calcium and phosphate levels and disturbances of its control mechanisms can lead to a variety of diseases. The insulin-sensitizing adipokine adiponectin is renoprotective and accelerates functional recovery following renal ... ...

Abstract	The kidney controls systemic calcium and phosphate levels and disturbances of its control mechanisms can lead to a variety of diseases. The insulin-sensitizing adipokine adiponectin is renoprotective and accelerates functional recovery following renal injury. However, unlike other adipokines, adiponectin is reduced in obesity. High adiponectin levels are also correlated with bone loss, suggestive of an additional action in mineral metabolism. Using knockout, wild-type, and adiponectin-overexpressing transgenic mice, we sought to identify the mechanistic basis for adiponectin's ability to regulate calcium and phosphate balance at the level of the kidney. Adiponectin knockout mice exhibited lower serum calcium, lower urinary calcium excretion, and markedly lower serum fibroblast growth factor 23 (FGF23) levels, although circulating klotho concentrations were significantly higher than in wild-type littermates. The transgenic mice exhibited lower bone mass and strength, particularly compared to adiponectin knockout mice. The transgenic mice were hyper-responsive to a 2% phosphate-enriched diet, exhibiting 2-fold higher serum FGF23 and concomitantly higher fractional phosphate excretion. These mice also excreted more calcium with calcium-enriched diet and had less renal klotho protein expression. In contrast, the knockout mice exhibited a smaller increase in FGF23 and maintained elevated klotho levels on both mineral challenges. Kidney-specific adiponectin expression in doxycycline-inducible adiponectin mice and adiponectin addition in vitro confirmed adiponectin's ability to reduce tubular epithelial cell klotho secretion. Thus, adiponectin alters calcium and phosphate balance and renal mineral excretion, in part, through klotho. This work highlights the profound effects of adipose tissue on renal function and has identified a new mechanism by which adiponectin may regulate bone mass.
MeSH term(s)	Adiponectin/deficiency ; Adiponectin/genetics ; Adiponectin/metabolism ; Animals ; Biomechanical Phenomena ; Calcium, Dietary/blood ; Calcium, Dietary/metabolism ; Calcium, Dietary/urine ; Collagen/metabolism ; Dogs ; Femur/metabolism ; Fibroblast Growth Factor-23 ; Fibroblast Growth Factors/blood ; Fibrosis ; Genotype ; Glucuronidase/blood ; Glucuronidase/genetics ; Homeostasis ; Hormones/blood ; Kidney/metabolism ; Kidney/pathology ; Kidney Tubules/metabolism ; Klotho Proteins ; Madin Darby Canine Kidney Cells ; Male ; Mice, Knockout ; Osteogenesis ; Phenotype ; Phosphates/blood ; Phosphates/metabolism ; Phosphates/urine ; Phosphorus, Dietary/blood ; Phosphorus, Dietary/metabolism ; Phosphorus, Dietary/urine ; Renal Elimination ; Spine/metabolism ; Transfection
Chemical Substances	Adiponectin ; Adipoq protein, mouse ; Calcium, Dietary ; Fgf23 protein, mouse ; Hormones ; Phosphates ; Phosphorus, Dietary ; Fibroblast Growth Factors (62031-54-3) ; Fibroblast Growth Factor-23 (7Q7P4S7RRE) ; Collagen (9007-34-5) ; Glucuronidase (EC 3.2.1.31) ; Klotho Proteins (EC 3.2.1.31)
Language	English
Publishing date	2016-11-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2016.09.016
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Article: Na+/H+ exchangers: physiology and link to hypertension and organ ischemia.

Bobulescu, I Alexandru / Di Sole, Francesca / Moe, Orson W

Current opinion in nephrology and hypertension

2005 Volume 14, Issue 5, Page(s) 485–494

Abstract: Purpose of review: Na/H exchangers (NHEs) are ubiquitous proteins with a very wide array of physiological functions, and they are summarized in this paper in view of the most recent advances. Hypertension and organ ischemia are two disease states of ... ...

Abstract	Purpose of review: Na/H exchangers (NHEs) are ubiquitous proteins with a very wide array of physiological functions, and they are summarized in this paper in view of the most recent advances. Hypertension and organ ischemia are two disease states of paramount importance in which NHEs have been implicated. The involvement of NHEs in the pathophysiology of these disorders is incompletely understood. This paper reviews the principal findings and current hypotheses linking NHE dysfunction to hypertension and ischemia. Recent findings: With the advent of large-scale sequencing projects and powerful in-silico analyses, we have come to know what is most likely the entire mammalian NHE gene family. Recent advances have detailed the roles of NHE proteins, exploring new functions such as anchoring, scaffolding and pH regulation of intracellular compartments. Studies of NHEs in disease models, even though not conclusive to date, have contributed new evidence on the interplay of ion transporters and the delicate ion balances that may become disrupted. Summary: This paper provides the interested reader with a concise overview of NHE physiology, and aims to address the implication of NHEs in the pathophysiology of hypertension and organ ischemia in light of the most recent literature.
MeSH term(s)	Animals ; Brain Ischemia/etiology ; Brain Ischemia/genetics ; Brain Ischemia/physiopathology ; Disease Models, Animal ; Humans ; Hypertension/etiology ; Hypertension/genetics ; Hypertension/physiopathology ; Ischemia/etiology ; Ischemia/genetics ; Ischemia/physiopathology ; Kidney/blood supply ; Kidney/physiopathology ; Mice ; Models, Biological ; Myocardial Ischemia/etiology ; Myocardial Ischemia/genetics ; Myocardial Ischemia/physiopathology ; Reperfusion Injury/genetics ; Reperfusion Injury/physiopathology ; Sodium-Hydrogen Exchangers/genetics ; Sodium-Hydrogen Exchangers/physiology
Chemical Substances	Sodium-Hydrogen Exchangers
Language	English
Publishing date	2005-07-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	1151092-4
ISSN	1535-3842 ; 1062-4821 ; 1062-4813
ISSN (online)	1535-3842
ISSN	1062-4821 ; 1062-4813
DOI	10.1097/01.mnh.0000174146.52915.5d
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Zs.A 3686: Show issues

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Article ; Online: Renal ammonium excretion after an acute acid load: blunted response in uric acid stone formers but not in patients with type 2 diabetes.

Bobulescu, I Alexandru / Maalouf, Naim M / Capolongo, Giovanna / Adams-Huet, Beverley / Rosenthal, Tara R / Moe, Orson W / Sakhaee, Khashayar

American journal of physiology. Renal physiology

2013 Volume 305, Issue 10, Page(s) F1498–503

Abstract: Idiopathic uric acid nephrolithiasis is characterized by elevated urinary net acid excretion and insufficient buffering by ammonium, resulting in excessively acidic urine and titration of the relatively soluble urate anion to insoluble uric acid. ... ...

Abstract	Idiopathic uric acid nephrolithiasis is characterized by elevated urinary net acid excretion and insufficient buffering by ammonium, resulting in excessively acidic urine and titration of the relatively soluble urate anion to insoluble uric acid. Patients with type 2 diabetes have similar changes in urinary pH, net acid excretion, and ammonium in 24-h urine collections at baseline, even after controlling for dietary factors, and are at increased risk for uric acid nephrolithiasis. However, not all patients with type 2 diabetes develop kidney stones, suggesting that uric acid stone formers may have additional urinary defects, perhaps not apparent at baseline. We performed a metabolic study of 14 patients with idiopathic uric acid nephrolithiasis, 13 patients with type 2 diabetes, and 8 healthy control subjects of similar body mass index. After equilibration on a fixed diet for 5 days, subjects were given a single oral acid load (50 meq ammonium chloride), and urine was collected hourly for 4 h. Uric acid stone formers had a lower ammonium excretory response to acute acid loading compared with diabetic and nondiabetic nonstone formers, suggesting that an ammonium excretory defect unique to uric acid stone formers was unmasked by the acid challenge. The Zucker diabetic fatty rat also did not show impaired urinary ammonium excretion in response to acute acid challenge. A blunted renal ammonium excretory response to dietary acid loads may contribute to the pathogenesis of idiopathic uric acid nephrolithiasis.
MeSH term(s)	Adult ; Aged ; Ammonium Chloride/administration & dosage ; Ammonium Chloride/urine ; Animals ; Biomarkers/blood ; Biomarkers/urine ; Body Mass Index ; Case-Control Studies ; Diabetes Mellitus, Type 2/blood ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/urine ; Diet ; Disease Models, Animal ; Female ; Humans ; Hydrogen-Ion Concentration ; Kidney/metabolism ; Kidney Calculi/blood ; Kidney Calculi/etiology ; Kidney Calculi/urine ; Male ; Middle Aged ; Rats ; Rats, Zucker ; Time Factors ; Uric Acid/urine
Chemical Substances	Biomarkers ; Ammonium Chloride (01Q9PC255D) ; Uric Acid (268B43MJ25)
Language	English
Publishing date	2013-09-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00374.2013
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Article ; Online: Reduction of renal triglyceride accumulation: effects on proximal tubule Na+/H+ exchange and urinary acidification.

Bobulescu, I Alexandru / Dubree, Michele / Zhang, Jianning / McLeroy, Paul / Moe, Orson W

American journal of physiology. Renal physiology

2009 Volume 297, Issue 5, Page(s) F1419–26

Abstract: One main pathophysiological mechanism underlying the increased risk for uric acid nephrolithiasis in humans with the metabolic syndrome is the excretion of unduly acidic urine, in part because of reduced excretion of the main urinary buffer, ammonium. ... ...

Abstract	One main pathophysiological mechanism underlying the increased risk for uric acid nephrolithiasis in humans with the metabolic syndrome is the excretion of unduly acidic urine, in part because of reduced excretion of the main urinary buffer, ammonium. The Zucker diabetic fatty (ZDF) rat, an established rodent model of the metabolic syndrome, has similar urinary abnormalities, attributed in part to lower expression and activity of the principal mediator of proximal tubule ammonium excretion, brush-border membrane Na+/H+ exchanger 3 (NHE3). These defects are associated with renal tubular steatosis in ZDF rats, but the causal relationship between renal steatosis and defective urinary acidification has not been investigated in vivo. We hypothesized that reduction of renal steatosis would commensurately normalize urinary acidification parameters. We treated ZDF rats with thiazolidinediones to reduce nonadipose tissue steatosis. Four weeks of treatment reduced renal triglyceride accumulation and restored urinary acidification parameters in ZDF rats to levels comparable to their lean littermates; urinary acidification was not affected by treatment in lean rats. To further document the direct effects of fat, we showed that functional abnormalities induced by fat loading in a cell culture model of proximal tubule steatosis and lipotoxicity can be reversed by fat removal but not by thiazolidinediones alone. Together, these findings support the causative role of renal steatosis in the pathogenesis of urinary acidification defects, demonstrate reversibility upon lipid removal, and highlight a potential therapeutic strategy for renal abnormalities in the metabolic syndrome.
MeSH term(s)	Acids/urine ; Adipose Tissue/metabolism ; Animals ; Cells, Cultured ; Fatty Acids, Nonesterified/blood ; Kidney/metabolism ; Kidney Tubules, Proximal/metabolism ; Microvilli/metabolism ; Opossums ; PPAR gamma/agonists ; Rats ; Rats, Zucker ; Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers/metabolism ; Thiazolidinediones/pharmacology ; Triglycerides/metabolism
Chemical Substances	Acids ; Fatty Acids, Nonesterified ; PPAR gamma ; SLC9A3 protein, human ; Slc9a3 protein, rat ; Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers ; Thiazolidinediones ; Triglycerides
Language	English
Publishing date	2009-08-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00177.2009
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Article ; Online: Characterization of the sodium/hydrogen exchanger NHA2.

Fuster, Daniel G / Zhang, Jianning / Shi, Mingjun / Bobulescu, I Alexandru / Andersson, Stefan / Moe, Orson W

Journal of the American Society of Nephrology : JASN

2008 Volume 19, Issue 8, Page(s) 1547–1556

Abstract: Cation/proton exchange has been recognized for decades in mammalian mitochondria, but the exchanger proteins have eluded identification. In this study, a cDNA from a human brain library, previously designated NHA2 in the genome, was cloned and ... ...

Abstract	Cation/proton exchange has been recognized for decades in mammalian mitochondria, but the exchanger proteins have eluded identification. In this study, a cDNA from a human brain library, previously designated NHA2 in the genome, was cloned and characterized. The NHA2 transcript bears more similarity to prokaryotic than known eukaryotic sodium/proton exchangers, but it was found to be expressed in multiple mammalian organs and cultured cells. A mAb to NHA2 was generated and found to label an approximately 55-kD native protein in multiple tissues and cell lines. The specificity of this antibody was confirmed by demonstrating the loss of the native NHA2 band on immunoblots when cultured cells were treated with NHA2-specific small interfering RNA. Although NHA2 protein was detected in multiple organs, within each, its expression was restricted to specific cell types. In the kidney, co-localization with calbindin 28k and reverse transcription-PCR of microdissected tubules revealed that NHA2 is limited to the distal convoluted tubule. In cell lines, native NHA2 was localized both to the plasma membrane and to the intracellular compartment; immunogold electron microscopy of rat distal convoluted tubule demonstrated NHA2 predominantly but not exclusively on the inner mitochondrial membrane. Furthermore, co-sedimentation of NHA2 antigen and mitochondrial membranes was observed with differential centrifugation, and two mitochondrial markers co-localized with NHA2 in cultured cells. Regarding function, human NHA2 reversed the sodium/hydrogen exchanger-null phenotype when expressed in sodium/hydrogen exchanger-deficient yeast and restored the ability to defend high salinity in the presence of acidic extracellular pH. In summary, NHA2 is a ubiquitous mammalian sodium proton/exchanger that is restricted to the distal convoluted tubule in the kidney.
MeSH term(s)	Amino Acid Sequence ; Antiporters/metabolism ; Cell Membrane/metabolism ; Humans ; Intracellular Space/metabolism ; Kidney Tubules, Distal/metabolism ; Molecular Sequence Data ; Tissue Distribution
Chemical Substances	Antiporters ; SLC9B2 protein, human
Language	English
Publishing date	2008-05-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2007111245
Database	MEDical Literature Analysis and Retrieval System OnLINE

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