Expression of the canalicular sulfate transport system in Xenopus laevis oocytes

Bissig, Marc; Hagenbuch, B.; Meier, Peter J.

doi:10.1016/0168-8278(90)91367-6

Cited by 57 publications

(139 citation statements)

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“…The SO 4 2-/anion exchange system that transports various anions including oxalate was demonstrated in the sinusoidal (114,115,121 membrane of rat hepatocytes (129). In support of these fi ndings, Sat-1, an exchanger of SO 4 2-and an oxalate, was localized in rats to the hepatocyte sinusoidal membrane (116,117,130). Recent transport studies on Sat-1 expressing oocytes demonstrated that Sat-1 can exchange SO 4 2-or HCO 3 -for oxalate in both directions, but the affi nity for oxalate is lower than for counter anions.…”

Section: Oxalate-handling Transporters and Their Role In Hyperoxalurimentioning

confidence: 52%

“…A transporter with similar properties was fi nally cloned from rat liver. cDNA encoded for the ~75 kDa SO 4 2-transporter, Sat-1 (130). The expression of rat renal sulfate transport systems in X. laevis oocytes proved that Sat-1 mediated Na + -independent SO 4 2-transport in the proximal tubule BLM (143).…”

Section: Figure 3 Transporters Along the Rodent Gastrointestinal Tracmentioning

confidence: 99%

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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: Oxalate-handling Transporters and Their Role In Hyperoxalurimentioning

confidence: 52%

Section: Figure 3 Transporters Along the Rodent Gastrointestinal Tracmentioning

confidence: 99%

Oxalate: From the Environment to Kidney Stones

Brzica

Breljak

Burckhardt

et al. 2013

Archives of Industrial Hygiene and Toxicology

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“…In rats, mice, and humans, sat-1 mRNA was detected strongly in liver and kidney and weakly in brain, skeletal muscle, and in few other organs [3,24,39]. The protein from the rat liver has been expression-cloned and characterized in Xenopus oocytes [3].…”

Section: Introductionmentioning

confidence: 99%

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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“…Although ClC-2 was suggested as a likely candidate (10,11), recent reports have questioned the apical localization and role of ClC-2 in gastric acid secretion (12,13). SLC26 (human)/Slc26 (mouse) homologs are members of a conserved family of anion exchangers that display selective and limited tissue expression in epithelial cells (14)(15)(16)(17)(18)(19)(20)(21)(22). Several SLC26 members can function as chloride/bicarbonate exchangers.…”

mentioning

confidence: 99%