Sulfate homeostasis, NaSi-1 cotransporter, and SAT-1 exchanger expression in chronic renal failure in rats

Fernandes, Isabelle; Laouari, Denise; Tutt, P; Hampson, Geeta; Friedlander, Gérard; Silve, Caroline

doi:10.1046/j.1523-1755.2001.00481.x

Cited by 26 publications

(16 citation statements)

References 33 publications

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“…During CRF, the expression of renal Sat-1 is signifi cantly reduced, which means that the active excretion of oxalate via the proximal tubule is also impaired. In addition, NaS-1, an important supplier of intracellular SO 4 2-for Sat-1-mediated oxalate transport, is also downregulated (156) (Figure 5.). 4 2-co-transport, mediated by the apical NaSi-1 (SLC13A1), which creates an outward SO 4 2-gradient that drives Sat-1-mediated SO 4 2-/oxalate exchange across the BLM.…”

Section: Figure 3 Transporters Along the Rodent Gastrointestinal Tracmentioning

confidence: 98%

Oxalate: From the Environment to Kidney Stones

Brzica

Breljak

Burckhardt

et al. 2013

Archives of Industrial Hygiene and Toxicology

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Oxalate urolithiasis (nephrolithiasis) is the most frequent type of kidney stone disease. Epidemiological research has shown that urolithiasis is approximately twice as common in men as in women, but the underlying mechanism of this sex-related prevalence is unclear. Oxalate in the organism partially originate from food (exogenous oxalate) and largely as a metabolic end-product from numerous precursors generated mainly in the liver (endogenous oxalate). Oxalate concentrations in plasma and urine can be modifi ed by various foodstuffs, which can interact in positively or negatively by affecting oxalate absorption, excretion, and/or its metabolic pathways. Oxalate is mostly removed from blood by kidneys and partially via bile and intestinal excretion. In the kidneys, after reaching certain conditions, such as high tubular concentration and damaged integrity of the tubule epithelium, oxalate can precipitate and initiate the formation of stones. Recent studies have indicated the importance of the SoLute Carrier 26 (SLC26) family of membrane transporters for handling oxalate. Two members of this family [Sulfate Anion Transporter 1 (SAT-1; SLC26A1) and Chloride/Formate EXchanger (CFEX; SLC26A6)] may contribute to oxalate transport in the intestine, liver, and kidneys. Malfunction or absence of SAT-1 or CFEX has been associated with hyperoxaluria and urolithiasis. However, numerous questions regarding their roles in oxalate transport in the respective organs and male-prevalent urolithiasis, as well as the role of sex hormones in the expression of these transporters at the level of mRNA and protein, still remain to be answered.

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Section: Figure 3 Transporters Along the Rodent Gastrointestinal Tracmentioning

confidence: 98%

Oxalate: From the Environment to Kidney Stones

Brzica

Breljak

Burckhardt

et al. 2013

Archives of Industrial Hygiene and Toxicology

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“…NaS1 mRNA and protein levels are down-regulated in the renal cortex by a variety of conditions, including: high sulfate diet (Markovich et al 1998), hypothyroidism (Sagawa et al 1999b), vitamin D depletion (Fernandes et al 1997), glucocorticoids (Lee et al 2000b), hypokalemia (Markovich et al 1999a), metabolic acidosis (Puttaparthi et al 1999) and non-steroidal anti-inflammatory drugs (Sagawa et al 1998a), and upregulated by low sulfate diet (Sagawa et al 1998b), thyroid hormone (Sagawa et al 1999b), vitamin D supplementation (Fernandes et al 1997), growth hormone (Sagawa et al 1999a), chronic renal failure (Fernandes et al 2001) and during post-natal growth (Markovich et al 1999b). NaS1 promoter studies showed up-regulation by vitamin D, thyroid hormone and the xenobiotic 3-methycholanthrene (Dawson and Markovich 2002;Lee et al 2005;Lee and Markovich 2004) and down-regulated by glucocorticoids (Beck and Markovich 2000).…”

Section: Cloning and Functional Characterization Of Renal Sulfate Tramentioning

confidence: 99%

Physiological Roles of Mammalian Sulfate Transporters NaS1 and Sat1

Markovich

2011

Arch. Immunol. Ther. Exp.

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This review summarizes the physiological roles of the renal sulfate transporters NaS1 (Slc13a1) and Sat1 (Slc26a1). NaS1 and Sat1 encode renal anion transporters that mediate proximal tubular sulfate reabsorption and thereby regulate blood sulfate levels. Targeted disruption of murine NaS1 and Sat1 leads to hyposulfatemia and hypersulfaturia. Sat1 null mice also exhibit hyperoxalemia, hyperoxaluria and calcium oxalate urolithiasis. Dysregulation of NaS1 and Sat1 leads to hypersulfaturia, hyposulfatemia and liver damage. Loss of Sat1 leads additionally to hyperoxaluria with hyperoxalemia, nephrocalcinosis and calcium oxalate urolithiasis. These data indicate that the renal anion transporters NaS1 and Sat1 are essential for sulfate and oxalate homeostasis, respectively.

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“…This reabsorption is mediated by Na + -dependent (NaSi-1) and Na + -independent processes (anion exchangers, such as CFEX/Slc26a6 and Slc26a7) at the brush-border and by sat-1 at the basolateral membrane [17,[31][32][33][34]37]. The physiological importance of the sat-1-mediated sulfate reabsorption has been confirmed in experimental chronic renal failure, which is associated with major downregulation of the renal sat-1 expression and significant increase of the fractional sulfate excretion [12].…”

Section: Introductionmentioning

confidence: 98%

The liver and kidney expression of sulfate anion transporter sat-1 in rats exhibits male-dominant gender differences

Brzica

Breljak

Krick

et al. 2008

Pflugers Arch - Eur J Physiol

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The sulfate anion transporter (sat-1, Slc26a1) has been cloned from rat liver, functionally characterized, and localized to the sinusoidal membrane in hepatocytes and basolateral membrane (BLM) in proximal tubules (PT). Here, we confirm previously described localization of sat-1 protein in rat liver and kidneys and report on gender differences (GD) in its expression by immunochemical, transport, and excretion studies in rats. The ∼85-kDa sat-1 protein was localized to the sinusoidal membrane in hepatocytes and BLM in renal cortical PT, with the maledominant expression. However, the real-time reversetranscription polymerase chain reaction data indicated no GD at the level of sat-1 mRNA. In agreement with the protein data, isolated membranes from both organs exhibited the male-dominant exchange of radiolabeled sulfate for oxalate, whereas higher oxalate in plasma and 24-h urine indicated higher oxalate production and excretion in male rats. Furthermore, the expression of liver, but not renal, sat-1 protein was: unaffected by castration, upregulated by ovariectomy, and downregulated by estrogen or progesterone treatment in males. Therefore, GD (males > females) in the expression of sat-1 protein in rat liver (and, possibly, kidneys) are caused by the female sexhormone-driven inhibition at the posttranscriptional level. The male-dominant abundance of sat-1 protein in liver may conform to elevated uptake of sulfate and extrusion of oxalate, causing higher plasma oxalate in males. Oxalate is then excreted by the kidneys via the basolateral sat-1 (males > females) and the apical CFEX (Slc26a6; GD unknown) in PT and eliminated in the urine (males > females), where it may contribute to the male-prevailing development of oxalate urolithiasis.

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Sulfate homeostasis, NaSi-1 cotransporter, and SAT-1 exchanger expression in chronic renal failure in rats

Cited by 26 publications

References 33 publications

Oxalate: From the Environment to Kidney Stones

Oxalate: From the Environment to Kidney Stones

Physiological Roles of Mammalian Sulfate Transporters NaS1 and Sat1

The liver and kidney expression of sulfate anion transporter sat-1 in rats exhibits male-dominant gender differences

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