ArticleAmerican journal of physiology. Cell physiology2005
Role of NBC1 in apical and basolateral HCO3- permeabilities and transendothelial HCO3- fluxes in bovine corneal endothelium.
Article in American journal of physiology. Cell physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Bicarbonate activates glycolysis and lactate production in corneal endothelial cells by increased pHExperimental eye research · 2020Article
- Corneal Endothelial Pump Coupling to Lactic Acid Efflux in the Rabbit and Mouse.Investigative ophthalmology & visual science · 2020Article
- A novel mutant NaThe Journal of physiology · 2016Article
- Fluid transport by the cornea endothelium is dependent on buffering lactic acid efflux.American journal of physiology. Cell physiology · 2016Article
- Mathematical modeling of acid-base physiology.Progress in biophysics and molecular biology · 2015Review
- Cation-coupled bicarbonate transporters.Comprehensive Physiology · 2014Review
- The divergence, actions, roles, and relatives of sodium-coupled bicarbonate transporters.Physiological reviews · 2013Review
- Molecular mechanisms underlying the corneal endothelial pump.Experimental eye research · 2012Review
- Functional Roles of Electrogenic Sodium Bicarbonate Cotransporter NBCe1 in Ocular Tissues.The open ophthalmology journal · 2012Article
- Bicarbonate, NBCe1, NHE, and carbonic anhydrase activity enhance lactate-H+ transport in bovine corneal endothelium.Investigative ophthalmology & visual science · 2011Article
- Soluble adenylyl cyclase mediates bicarbonate-dependent corneal endothelial cell protection.American journal of physiology. Cell physiology · 2011Article
- Knockdown of NBCe1 in vivo compromises the corneal endothelial pump.Investigative ophthalmology & visual science · 2010Article
- Dependence of cAMP meditated increases in Cl- and HCO(3)- permeability on CFTR in bovine corneal endothelial cells.Experimental eye research · 2008Article
- Effect of p27Kip1 inhibition on proliferation of bovine corneal endothelial cells by RNA interference.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2008Article
- Role of carbonic anhydrase IV in corneal endothelial HCO3- transport.Investigative ophthalmology & visual science · 2008Article
- Molecular expression and functional involvement of the bovine calcium-activated chloride channel 1 (bCLCA1) in apical HCO3- permeability of bovine corneal endothelium.Experimental eye research · 2006Article
- Transporters involved in regulation of intracellular pH in primary cultured rat brain endothelial cells.The Journal of physiology · 2006Article
- Potential applications for RNAi to probe pathogenesis and develop new treatments for ocular disorders.Gene therapy · 2006Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Corneal transparency and hydration control are dependent on HCO(3)(-) transport properties of the corneal endothelium. Recent work (13) suggested the presence of an apical 1Na(+)-3HCO(3)(-) cotransporter (NBC1) in addition to a basolateral 1Na(+)-2HCO(3)(-) cotransporter. We examined whether the NBC1 cotransporter contributes significantly to basolateral or apical HCO(3)(-) permeability and whether the cotransporter participates in transendothelial net HCO(3)(-) flux in cultured bovine corneal endothelium. NBC1 protein expression was reduced using small interfering RNA (siRNA). Immunoblot analysis showed that 5-15 nM siRNA decreased NBC1 expression by 80-95%, 4 days posttransfection. Apical and basolateral HCO(3)(-) permeabilities were determined by measuring the rate of pH(i) change when HCO(3)(-) was removed from the bath under constant pH or constant CO(2) conditions. Using either protocol, we found that cultures treated with NBC1 siRNA had sixfold lower basolateral HCO(3)(-) permeability than untreated or siCONTROL siRNA-treated cells. Apical HCO(3)(-) permeability was unaffected by NBC1 siRNA treatment. Net non-steady-state HCO(3)(-) flux was 0.707 +/- 0.009 mM.min(-1).cm(2) in the basolateral-to-apical direction and increased to 1.74 +/- 0.15 when cells were stimulated with 2 muM forskolin. Treatment with 5 nM siRNA decreased basolateral-to-apical flux by 67%, whereas apical-to-basolateral flux was unaffected, significantly decreasing net HCO(3)(-) flux to 0.236 +/- 0.002. NBC1 siRNA treatment or 100 muM ouabain also eliminated steady-state HCO(3)(-) flux, as measured by apical compartment alkalinization. Collectively, reduced basolateral HCO(3)(-) permeability, basolateral-to-apical fluxes, and net HCO(3)(-) flux as a result of reduced expression of NBC1 indicate that NBC1 plays a key role in transendothelial HCO(3)(-) flux and is functional only at the basolateral membrane.
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