ArticleInvestigative ophthalmology & visual science2013
Ion transport function of SLC4A11 in corneal endothelium.
Article in Investigative ophthalmology & visual science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 73 citations in OpenAlex.
- Mutations in the TMCO3 Gene are Associated with Cornea Guttata and Anterior Polar Cataract.Scientific reports · 2016Trial
- Complete SLC4A11 Detection in Saudi Congenital Hereditary Endothelial Dystrophy: A Transmembrane Glycine Hotspot and a Recurrent Splice Donor Allele in Consanguineous Patients.International journal of molecular sciences · 2026Article
- Cryo-EM structures and transport mechanism of human multifunctional transporter BTR1.Protein & cell · 2026Article
- Review
- KInternational journal of molecular sciences · 2024Article
- NHFrontiers in physiology · 2024Article
- Pathogenicity and Function Analysis of Two Novel SLC4A11 Variants in Patients With Congenital Hereditary Endothelial Dystrophy.Translational vision science & technology · 2023Article
- The roles of autophagy and mitophagy in corneal pathology: current knowledge and future perspectives.Frontiers in medicine · 2023Review
- TGF-β-Mediated Modulation of Cell-Cell Interactions in Postconfluent Maturing Corneal Endothelial Cells.Investigative ophthalmology & visual science · 2022Article
- The HCells · 2022Review
- RNA sequencing uncovers alterations in corneal endothelial metabolism, pump and barrier functions of Slc4a11 KO mice.Experimental eye research · 2022Article
- Mitochondrial Targeting of the Ammonia-Sensitive Uncoupler SLC4A11 by the Chaperone-Mediated Carrier Pathway in Corneal Endothelium.Investigative ophthalmology & visual science · 2021Article
- "SLC-omics" of the kidney: solute transporters along the nephron.American journal of physiology. Cell physiology · 2021Review
- Animal models of corneal endothelial dysfunction to facilitate development of novel therapies.Annals of translational medicine · 2021Review
- Genetic mutations and molecular mechanisms of Fuchs endothelial corneal dystrophy.Eye and vision (London, England) · 2021Review
- Downregulated ATP6V1B1 expression acidifies the intracellular environment of cancer cells leading to resistance to antibody-dependent cellular cytotoxicity.Cancer immunology, immunotherapy : CII · 2021Article
- Harboyan syndrome: novel SLC4A11 mutation, clinical manifestations, and outcome of corneal transplantation.Journal of human genetics · 2021Observational
- pH dependence of the Slc4a11-mediated HAmerican journal of physiology. Cell physiology · 2020Article
- SLC4A11 function: evidence for HAmerican journal of physiology. Cell physiology · 2020Article
- Molecular Mechanisms of Fuchs and Congenital Hereditary Endothelial Corneal Dystrophies.Reviews of physiology, biochemistry and pharmacology · 2020Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
purposeMutations in SLC4A11, a member of the SLC4 superfamily of bicarbonate transporters, give rise to corneal endothelial cell dystrophies. SLC4A11 is a putative Na⁺ borate and Na⁺:OH⁻ transporter. Therefore we ask whether SLC4A11 in corneal endothelium transports borate (B[OH]₄⁻), bicarbonate (HCO3⁻), or hydroxyl (OH⁻) anions coupled to Na⁺.
methodsSLC4A11 expression in cultured primary bovine corneal endothelial cells (BCECs) was determined by semiquantitative PCR, SDS-PAGE/Western blotting, and immunofluorescence staining. Ion transport function was examined by measuring intracellular pH (pHi) or Na⁺ ([Na⁺](i)) in response to Ringer solutions with/without B(OH)₄⁻ or HCO₃⁻ after overexpressing or small interfering RNA (siRNA) silencing of SLC4A11.
resultsSLC4A11 is localized to the basolateral membrane in BCEC. B(OH)₄⁻ (2.5-10 mM) in bicarbonate-free Ringer induced a rapid small acidification (0.01 pH unit) followed by alkalinization (0.05-0.1 pH unit), consistent with diffusion of boric acid into the cell followed by B(OH)₄⁻. However, the rate of B(OH)₄⁻-induced pHi change was unaffected by overexpression of SLC4A11. B(OH)₄⁻ did not induce significant changes in resting [Na⁺(i)] or the amplitude and rate of acidification caused by Na⁺ removal. siRNA-mediated knockdown of SLC4A11 (∼70%) did not alter pHi responses to CO₂/HCO₃⁻-rich Ringer, Na⁺-free induced acidification, or the rate of Na⁺ influx in the presence of bicarbonate. However, in the absence of bicarbonate, siSLC4A11 knockdown significantly decreased the rate (43%) and amplitude (48%) of acidification due to Na⁺ removal and recovery (53%) upon add-back. Additionally, the rate of acid recovery following NH₄⁺ prepulse was decreased significantly (27%) by SLC4A11 silencing.
conclusionsIn corneal endothelium, SLC4A11 displays robust Na⁺-coupled OH⁻ transport, but does not transport B(OH)₄⁻ or HCO₃⁻.
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