ArticleThe Journal of physiology2004
Slc26a6: a cardiac chloride-hydroxyl exchanger and predominant chloride-bicarbonate exchanger of the mouse heart.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
31 citing papers in PubMed, 84 citations in OpenAlex.
- Ablation of Slc26a6 Mitigates Myocardial Ischemia/Reperfusion Injury.Biomedicines · 2025Article
- Chloride/Multiple Anion Exchanger SLC26A Family: Systemic Roles of SLC26A4 in Various Organs.International journal of molecular sciences · 2024Review
- Acidic environments trigger intracellular H+-sensing FAK proteins to re-balance sarcolemmal acid-base transporters and auto-regulate cardiomyocyte pH.Cardiovascular research · 2022Article
- Molecular Characterization and RNA Interference Analysis of SLC26A10 FromFrontiers in physiology · 2022Article
- A Cardioplegic Solution with an Understanding of a Cardiochannelopathy.Antioxidants (Basel, Switzerland) · 2021Review
- The Fundamental Role of Bicarbonate Transporters and Associated Carbonic Anhydrase Enzymes in Maintaining Ion and pH Homeostasis in Non-Secretory Organs.International journal of molecular sciences · 2020Review
- Physiological and Pathological Functions of SLC26A6.Frontiers in medicine · 2020Review
- Importance of SLC26 Transmembrane Anion Exchangers in Sperm Post-testicular Maturation and Fertilization Potential.Frontiers in cell and developmental biology · 2019Review
- Enhanced Activity by NKCC1 and Slc26a6 Mediates Acidic pH and ClMediators of inflammation · 2019Article
- Electrophysiological properties of anion exchangers in the luminal membrane of guinea pig pancreatic duct cells.Pflugers Archiv : European journal of physiology · 2018Article
- Action Potential Shortening and Impairment of Cardiac Function by Ablation ofCirculation. Arrhythmia and electrophysiology · 2017Article
- RNA SEQ Analysis Indicates that the AE3 ClScientific reports · 2017Article
- Epidermal Growth Factor Receptor Silencing Blunts the Slow Force Response to Myocardial Stretch.Journal of the American Heart Association · 2016Article
- Functional interaction between bicarbonate transporters and carbonic anhydrase modulates lactate uptake into mouse cardiomyocytes.Pflugers Archiv : European journal of physiology · 2015Article
- Critical role of bicarbonate and bicarbonate transporters in cardiac function.World journal of biological chemistry · 2014Review
- Resistance to cardiomyocyte hypertrophy in ae3-/- mice, deficient in the AE3 Cl-/HCO3- exchanger.BMC cardiovascular disorders · 2014Article
- Transient complex I inhibition at the onset of reperfusion by extracellular acidification decreases cardiac injury.American journal of physiology. Cell physiology · 2014Article
- Molecular transport machinery involved in orchestrating luminal acid-induced duodenal bicarbonate secretion in vivo.The Journal of physiology · 2013Article
- Loss of the AE3 Cl(-)/HCO(-) 3 exchanger in mice affects rate-dependent inotropy and stress-related AKT signaling in heart.Frontiers in physiology · 2013Article
- K+-Cl- cotransporter-2 KCC2 in chicken cardiomyocytes.American journal of physiology. Cell physiology · 2012Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bicarbonate facilitate more than 50% of pH recovery in the acidotic myocardium, and have roles in cardiac hypertrophy and steady-state pH regulation. To determine which bicarbonate transporters are responsible for this activity, we measured the expression levels of all known HCO3(-)-anion exchange proteins in mouse heart, by quantitative real time RT-PCR. Bicarbonate-anion exchangers are members of either the SLC4A or the SLC26A gene families. In neonatal and adult myocardium, AE1 (Slc4a1), AE2 (Slc4a2), AE3 (Slc4a3) (AE3fl and AE3c variants), Slc26a3 and Slc26a6 were expressed. Adult hearts expressed Slc26a3 and Slc4a1-3 mRNAs at similar levels, while Slc26a6 mRNA was about seven-fold higher than AE3, which was more abundant than any other. Immunohistochemistry revealed that Slc26a6 and AE3 are present in the plasma membrane of ventricular myocytes. Slc26a6 expression levels were higher in ventricle than atrium, whereas AE3 was detected only in ventricle. Cl(-)-HCO(3)(-) and Cl(-)-OH(-) exchange activity of SLC26A6 and AE3 were investigated in transfected HEK293 cells, using intracellular fluorescence measurements of 2',7'-bis (2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF), to monitor intracellular pH (pH(i)). Rates of pH(i) change were measured under HCO3(-)-containing (Cl(-)-HCO(3)(-)) or nominally HCO3(-)-free (Cl(-)-OH(-)) conditions. HCO3(-) fluxes were similar for cells expressing AE3fl, SLC26A6 or Slc26a3, suggesting that they have similar transport activity. However, only SLC26A6 and Slc26a3 functioned as Cl(-)-OH(-) exchangers. Activation of alpha-adrenergic receptors, which stimulates protein kinase C, inhibited SLC26A6 Cl(-)-HCO(3)(-) exchange activity. We conclude that Slc26a6 is the predominant Cl(-)-HCO(3)(-) and Cl(-)-OH(-) exchanger of the myocardium and that Slc26a6 is negatively regulated upon alpha-adrenergic stimulation.
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Registered trials
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