Differential Regulation of Mouse Kidney Sodium-Dependent Transporters mRNA by Cadmium

Tabatabai, Niloofar M.; Blumenthal, Samuel S.; Lewand, Donna L.; Petering, David H.

doi:10.1006/taap.2001.9321

Cited by 30 publications

(44 citation statements)

References 28 publications

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“…To check for the specific renal expression of Sglt2, we extracted RNA from a variety of mouse tissues and carried out RT-PCR using oligonucleotide primers specific for mouse sglt2 cDNA (10). A 707-bp product representing the fragment expected from the published mouse sglt2 cDNA sequence (GenBank accession no.…”

Section: Sglt2 Is Kidney Specific In Wild-type Micementioning

confidence: 99%

Specific Cre/Lox Recombination in the Mouse Proximal Tubule

Rubera¹,

Poujeol²,

Bertin³

et al. 2004

Journal of the American Society of Nephrology

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Abstract. The present work reports for the first time the construction of a transgenic mouse strain with specific expression of Cre recombinase in the kidney proximal tubule. A Cre/loxP strategy was developed using sglt2 promoter to drive Cre recombinase expression in transgenic mice. The mouse sglt2 5' region consisting of the first exon, the first intron, and part of the second exon was cloned upstream of a nucleotide sequence encoding the Cre recombinase. Transgenic mice were generated by pronuclear injection, and tissue specificity of Cre expression was analyzed using reverse transcription-PCR. The iL1-sglt2-Cre mouse line scored positive for kidney transcription of Cre but not for the other tissues analyzed. Within the kidney, Cre transcripts were demonstrated to be restricted to the proximal tubule only. iL1-sglt2-Cre mice were bred with ROSA26-LacZ reporter mice that contained a loxP-flanked stop sequence upstream of the LacZ gene. X-gal staining and immunohistochemistry using specific antibodies (anti-megalin, anti-Tamm-Horsfall, anti-NaCl co-transporter, and anti-aquaporin 2) revealed that sglt2 drives Cre functional expression specifically in proximal tubules. The iL1-sglt2-Cre mouse therefore represents a powerful tool for Cre-LoxP-mediated conditional expression in the renal proximal tubule.

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Section: Sglt2 Is Kidney Specific In Wild-type Micementioning

confidence: 99%

Specific Cre/Lox Recombination in the Mouse Proximal Tubule

Rubera¹,

Poujeol²,

Bertin³

et al. 2004

Journal of the American Society of Nephrology

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“…Cd at a concentration of 5 μ M induces mostly MT synthesis, and it induces mostly HO-1 at concentrations between 10 μ M and 20 μ M (Garrett et al 1998;Klaassen et al 1999;Hill-Kapturczak et al 2003). Cd induces the specific subtype of sodium-dependent glucose transporter while it suppresses two other subtypes (Tabatabai et al 2001). Some of these Cd inducible proteins are known to participate in defense mechanism that provides protection against injury.…”

Section: Molecular Mechanisms Underlying Renal CD Toxicitymentioning

confidence: 99%

Kidney Dysfunction and Hypertension: Role for Cadmium, P450 and Heme Oxygenases?

Satarug

Nishijo

Lasker

et al. 2006

Tohoku J. Exp. Med.

100

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“…Glucose is freely filtered by the glomerulus, and reabsorption occurs predominantly on the brushborder membrane of the convoluted segment of the proximal tubule by specific transporter proteins. More distal segments reabsorb almost all of the remainder, resulting in a fractional glucose excretion of Ͻ0.1% (44,45). The sodium-dependent cotransporters (SGLTs), consisting of three subtypes, couple the uphill reabsorption of glucose from the renal tubule lumen with the downhill transport of sodium (19,20).…”

mentioning

confidence: 99%

“…Because this transporter has a Na ϩ -glucose stoichiometry of 2:1, it can generate a far larger glucose gradient across the apical membrane (45). In addition to SGLT1 and SGLT2, another closely related low-affinity sodiumglucose transporter, SGLT3, originally named SAAT1, has been identified in the proximal tubule, coupling two Na ϩ to one glucose molecule (15,44,45). Once inside the cell, glucose exits across the basolateral membrane via the insulindependent GLUT transporters, which are Na ϩ independent and move glucose by facilitated diffusion.…”

mentioning

confidence: 99%

“…Like the apical SGLTs, the basolateral GLUTs differ between early and late proximal tubule segments, with GLUT2 in the early and GLUT1 in the late proximal tubule (4). The electrochemical potential gradient for powering Na ϩ -glucose symporter is restored when transported sodium is returned to the blood stream via the basolateral Na ϩ -K ϩ -ATPase along the whole nephron (44,45). Reports of altered glucose transporter expression in extrarenal tissue during endotoxemia directed our interest onto the regulation of renal tubular glucose transporters during experimental sepsis (51,52).…”

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confidence: 99%

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Regulation of renal glucose transporters during severe inflammation

Schmidt¹,

Höcherl²,

Bucher³

2007

American Journal of Physiology-Renal Physiology

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Schmidt C, Höcherl K, Bucher M. Regulation of renal glucose transporters during severe inflammation. Am J Physiol Renal Physiol 292: F804 -F811, 2007. First published October 10, 2006; doi:10.1152/ajprenal.00258.2006.-Severe sepsis is accompanied by acute renal failure (ARF) with renal tubular dysfunction and glucosuria. In this study, we aimed to determine the regulation of renal tubular glucose transporters during severe experimental inflammation. Male C57BL/6J mice were injected with LPS or proinflammatory cytokines, and renal perfusion, glomerular filtration rate (GFR), fractional glucose excretion, and expression of tubular glucose transporters were determined. We found a decreased plasma glucose concentration with impaired renal tissue perfusion and GFR and increased fractional glucose excretion associated with decreased expression of SGLT2, SGLT3, and GLUT2 after LPS injection. Similar alterations were observed after application of TNF-␣, IL-1␤, IL-6, or IFN-␥. To clarify the role of proinflammatory cytokines, we performed LPS injections in knockout mice with deficiencies for TNF-␣, IL-1 receptor type 1, IFN-␥, or IL-6 as well as LPS injections in glucocorticoidtreated wild-type mice. LPS-induced alterations of glucose transporters also were present in single-cytokine knockout mice. In contrast, glucocorticoid treatment clearly attenuated LPS-induced changes in renal glucose transporter expression and improved GFR and fractional glucose excretion. LPS-induced decrease of renal perfusion was not improved by glucocorticoids, indicating a minor role of ischemia in the development of septic renal dysfunction. Our results demonstrate modifications of tubular glucose transporters during severe inflammation that are probably mediated by proinflammatory cytokines and account for the development of ARF with increased fractional glucose excretion. In addition, our findings provide an explanation why single anti-cytokine strategies fail in the therapy of septic patients and contribute to an understanding of the beneficial effects of glucocorticoids on septic renal dysfunction.

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Differential Regulation of Mouse Kidney Sodium-Dependent Transporters mRNA by Cadmium

Cited by 30 publications

References 28 publications

Specific Cre/Lox Recombination in the Mouse Proximal Tubule

Specific Cre/Lox Recombination in the Mouse Proximal Tubule

Kidney Dysfunction and Hypertension: Role for Cadmium, P450 and Heme Oxygenases?

Regulation of renal glucose transporters during severe inflammation

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