ArticleAmerican journal of physiology. Renal physiology2014
Insights into acidosis-induced regulation of SLC26A4 (pendrin) and SLC4A9 (AE4) transporters using three-dimensional morphometric analysis of β-intercalated cells.
Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Urinary sodium wasting and disrupted collecting duct function in mice with distal renal tubular acidosis mutations.Disease models & mechanisms · 2025Article
- Potential Theranostic Roles of SLC4 Molecules in Human Diseases.International journal of molecular sciences · 2023Review
- Signaling mechanisms in renal compensatory hypertrophy revealed by multi-omics.Nature communications · 2023Article
- The AE4 transporter mediates kidney acid-base sensing.Nature communications · 2023Article
- Ammonium chloride-induced acidosis exacerbates cystitis and pyelonephritis caused by uropathogenic E. coli.Physiological reports · 2022Article
- Activation of 2-oxoglutarate receptor 1 (OXGR1) by α-ketoglutarate (αKG) does not detectably stimulate Pendrin-mediated anion exchange in Xenopus oocytes.Physiological reports · 2022Article
- Activation of the Ae4 (Slc4a9) cation-driven ClAmerican journal of physiology. Gastrointestinal and liver physiology · 2021Article
- A guide to plasma membrane solute carrier proteins.The FEBS journal · 2021Review
- Acute regulated expression of pendrin in human urinary exosomes.Pflugers Archiv : European journal of physiology · 2018Article
- Single-tubule RNA-Seq uncovers signaling mechanisms that defend against hyponatremia in SIADH.Kidney international · 2018Article
- Metabolic acidosis stimulates the production of the antimicrobial peptide cathelicidin in rabbit urine.American journal of physiology. Renal physiology · 2017Article
- SDF1 induction by acidosis from principal cells regulates intercalated cell subtype distribution.The Journal of clinical investigation · 2015Article
- pH-sensitive expression of calcium-sensing receptor (CaSR) in type-B intercalated cells of the cortical collecting ducts (CCD) in mouse kidney.Clinical and experimental nephrology · 2015Article
- Distinct α-intercalated cell morphology and its modification by acidosis define regions of the collecting duct.American journal of physiology. Renal physiology · 2015Article
- The multiple roles of pendrin in the kidney.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2015Review
- Collecting duct intercalated cell function and regulation.Clinical journal of the American Society of Nephrology : CJASN · 2015Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The purpose of this study was to examine the three-dimensional (3-D) expression and distribution of anion transporters pendrin (SLC26A4) and anion exchanger (AE)4 (SLC4A9) in β-intercalated cells (β-ICs) of the rabbit cortical collecting duct (CCD) to better characterize the adaptation to acid-base disturbances. Confocal analysis and 3-D reconstruction of β-ICs, using identifiers of the nucleus and zona occludens, permitted the specific orientation of cells from normal, acidotic, and recovering rabbits, so that adaptive changes could be quantified and compared. The pendrin cap likely mediates apical Cl(-)/HCO3 (-) exchange, but it was also found beneath the zona occludens and in early endosomes, some of which may recycle back to the apical membrane via Rab11a(+) vesicles. Acidosis reduced the size of the pendrin cap, observed as a large decrease in cap volume above and below the zona occludens, and the volume of the Rab11a(+) apical recycling compartment. Correction of the acidosis over 12-18 h reversed these changes. Consistent with its proposed function in the basolateral exit of Na(+) via Na(+)-HCO3 (-) cotransport, AE4 was expressed as a barrel-like structure in the lateral membrane of β-ICs. Acidosis reduced AE4 expression in β-ICs, but this was rapidly reversed during the recovery from acidosis. The coordinate regulation of pendrin and AE4 during acidosis and recovery is likely to affect the magnitude of acid-base and possibly Na(+) transport across the CCD. In conclusion, acidosis induces a downregulation of AE expression in β-ICs and a diminished presence of pendrin in apical recycling endosomes.
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