Cation specificity and modes of the Na+:CO3(2-):HCO3- cotransporter in renal basolateral membrane vesicles

Soleimani, Manoocher; Lesoine, G A; Bergman, Julia; Aronson, Peter S.

doi:10.1016/s0021-9258(18)31503-5

Cited by 29 publications

(3 citation statements)

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“…23 An important finding of the present study was that Li + influx in hCMEC/D3 was significantly reduced by DIDS but was significantly increased by S0859, suggesting also the partic-ipation of NBCs in the transport of Li + in human brain endothelial cells.. It was reported that Li + has significantly inhibited the HCO 3 − -stimulated Na + influx in rabbit renal vesicles, 32 and Li + was regarded as 25% effective as Na + in regulating DIDS-sensitive HCO 3− -dependent acid extrusion in human NBCe1-overexpressed HEK293 cells. 33 NBCs would transport Na + (and/or Li + ) and HCO 3 − together into the hCMEC/D3 cells, but we observed a significant increase in Li + influx in hCMEC/D3 cells when incubated with S0859.…”

Section: ■ Discussionsupporting

confidence: 54%

Sodium Transporters Are Involved in Lithium Influx in Brain Endothelial Cells

et al. 2018

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Variability in drug response to lithium (Li) is poorly understood and significant, as only 40% of patients with bipolar disorder highly respond to Li. Li can be transported by sodium (Na) transporters in kidney tubules or red blood cells, but its transport has not been investigated at the blood-brain barrier (BBB). Inhibition and/or transcriptomic strategies for Na transporters such as NHE (SLC9), NBC (SLC4), and NKCC (SLC12) were used to assess their role on Li transport in human brain endothelial cells. Na-free buffer was also used to examine Na/Li countertransport (NLCT) activity. The BBB permeability of Li evaluated in the rat was 2% that of diazepam, a high passive diffusion lipophilic compound. Gene expression of several Na transporters was determined in hCMEC/D3 cells, human hematopoietic stem-cell-derived BBB models (HBLEC), and human primary brain microvascular endothelial cells (hPBMECs) and showed the following rank order with close expression profile: NHE1 > NKCC1 > NHE5 > NBCn1, while NHE2-4, NBCn2, and NBCe1-2 were barely detected. Li influx in hCMEC/D3 cells was increased in Na-free buffer by 3.3-fold, while depletion of chloride or bicarbonate had no effect. DMA (NHE inhibitor), DIDS (anionic carriers inhibitor), and bumetanide (NKCC inhibitor) decreased Li uptake significantly in hCMEC/D3 by 52, 51, and 47%, respectively, while S0859 (NBC inhibitor) increased Li influx 2.3-fold. Zoniporide (NHE1 inhibitor) and siRNA against NHE1 had no effect on Li influx in hCMEC/D3 cells. Our study shows that NHE1 and/or NHE5, NBCn1, and NKCC1 may play a significant role in the transport of Li through the plasma membrane of brain endothelial cells.

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Section: ■ Discussionsupporting

confidence: 54%

Sodium Transporters Are Involved in Lithium Influx in Brain Endothelial Cells

et al. 2018

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“…Previous studies reported the involvement of NBCs in Li transport in other tissues and cells. In rabbit renal vesicles, Li was found to inhibit the HCO 3 --stimulated Na influx [85]. In HEK293 cells over-expressed NBCe1, Li was shown to modulate DIDS-sensitive HCO 3 --dependent Na extrusion [86].…”

Section: Transport Mechanisms Of Lithium Across the Bbb And Bcsfbmentioning

confidence: 98%

The role of brain barriers in the neurokinetics and pharmacodynamics of lithium

Luo

Chevillard²,

Bellivier³

et al. 2021

Pharmacological Research

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“…In addition to the formation of molecular complexes inside the cell membrane, an important point might be what kind of transmembranous proteins interact with 4.1B in the renal proximal tubules. In S1-S2 renal proximal tubules, sodium bicarbonate cotransporter1 (NBC1) is well known to be a major transporter for HCO 3 2 reabsorption across the basolateral membranes, and contributes significantly to Na 1 reabsorption (Soleimani et al 1991). NBC1 is a member of the SLC4 family of bicarbonate transporters, which comprises at least eight genes (Romero et al 2004).…”

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confidence: 99%

Interaction of Membrane Skeletal Protein, Protein 4.1B and p55, and Sodium Bicarbonate Cotransporter1 in Mouse Renal S1-S2 Proximal Tubules

Terada

Ohno

Saitoh

et al. 2007

J Histochem Cytochem.

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Our recent studies demonstrated the localization of protein 4.1B, a member of the 4.1 skeletal membrane proteins, to the basolateral membranes of the S1-S2 renal proximal tubules. In the present studies, we investigated the presence of binding partners that could form a molecular complex with the 4.1B protein. Immunohistochemistry revealed the localization of p55, a membrane-associated guanylate kinase, and the sodium bicarbonate cotransporter1 (NBC1), to the basolateral membrane domain of S1-S2 in mouse renal proximal tubules. Using immunoprecipitation of kidney lysates with anti-p55 antibody, a positive band was blotted with anti-4.1B antibody. GST fusion proteins including the NBC1 and 4.1B regions were confirmed to bind with each other by electrophoresis after mixing. Both NBC1- and 4.1B-specific bands were detected in renal protein mixtures immunoprecipated by either anti-4.1B- or NBC1-specific antibodies. It is likely that NBC1, 4.1B, and p55 form a molecular complex in the basolateral membrane of the kidney S1-S2 proximal tubules. We propose that the 4.1B-containing membrane skeleton may play a role in regulating the Na(+) and HCO(3)(-) reabsorption in S1-S2 proximal tubules.

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Cation specificity and modes of the Na+:CO3(2-):HCO3- cotransporter in renal basolateral membrane vesicles

Cited by 29 publications

References 0 publications

Sodium Transporters Are Involved in Lithium Influx in Brain Endothelial Cells

Sodium Transporters Are Involved in Lithium Influx in Brain Endothelial Cells

The role of brain barriers in the neurokinetics and pharmacodynamics of lithium

Interaction of Membrane Skeletal Protein, Protein 4.1B and p55, and Sodium Bicarbonate Cotransporter1 in Mouse Renal S1-S2 Proximal Tubules

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