ArticlePflugers Archiv : European journal of physiology2013
Role of bestrophin-1 in store-operated calcium entry in retinal pigment epithelium.
Article in Pflugers Archiv : European journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 57 citations in OpenAlex.
- Evaluation of the Toxicity and Efficacy of an Adeno-Associated Viral Vector ExpressingHuman gene therapy · 2026Article
- CaActa physiologica (Oxford, England) · 2026Review
- Review of the clinical electrooculogram - Part 1: Mechanism of the Light-Rise.Documenta ophthalmologica. Advances in ophthalmology · 2026Review
- Gene Therapy Strategies for the Treatment of Bestrophinopathies.International journal of molecular sciences · 2025Review
- Unilateral best vitelliform macular dystrophy- a case series.Documenta ophthalmologica. Advances in ophthalmology · 2025Article
- Loss of Stim2 in zebrafish induces glaucoma-like phenotype.Scientific reports · 2024Article
- Choroidal Neovascularization Is Common in Best Vitelliform Macular Dystrophy and Plays a Role in Vitelliform Lesion Evolution.Ophthalmology. Retina · 2023Article
- Cellular and Molecular Mechanisms of Pathogenesis Underlying Inherited Retinal Dystrophies.Biomolecules · 2023Review
- Is white the right light for the clinical electrooculogram?Documenta ophthalmologica. Advances in ophthalmology · 2021Article
- Electrophysiological Properties of Endogenous Single CaInternational journal of molecular sciences · 2021Article
- Altered Protein Function Caused by AMD-associated Variant rs704 Links Vitronectin to Disease Pathology.Investigative ophthalmology & visual science · 2020Article
- Lessons learned from quantitative fundus autofluorescence.Progress in retinal and eye research · 2020Review
- Multimodal Imaging in Best Vitelliform Macular Dystrophy.Investigative ophthalmology & visual science · 2019Article
- Robust lysosomal calcium signaling through channel TRPML1 is impaired by lysosomal lipid accumulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Article
- Bestrophinopathy: An RPE-photoreceptor interface disease.Progress in retinal and eye research · 2017Review
- Bestrophin 1 and retinal disease.Progress in retinal and eye research · 2017Review
- Expression of anoctamins in retinal pigment epithelium (RPE).Pflugers Archiv : European journal of physiology · 2016Article
- High glucose promotes the migration of retinal pigment epithelial cells through increased oxidative stress and PEDF expression.American journal of physiology. Cell physiology · 2016Article
- Unilateral BEST1-Associated Retinopathy.American journal of ophthalmology · 2016Observational
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The retinal pigment epithelium (RPE) expresses bestrophin-1 where mutant bestrophin cause retinal degenerations. Overexpression of bestrophin-1 demonstrated Ca(2+)-dependent Cl(-) channel function, whereas the RPE in bestrophin-1 knockout or mutant bestrophin-1 knock-in mice showed no change in Cl(-) conductance. To account for these apparently mutually exclusive findings, we investigated the function of endogenously expressed bestrophin-1 in a short-time RPE cell culture system by means of immunocytochemistry, Ca(2+) imaging, and siRNA knockdown. Immunocytochemical quantification of bestrophin-1 localization demonstrated 2.5 times higher co-localization with the endoplasmic reticulum (ER) Ca(2+)-sensor protein, Stim-1, than with the membrane protein β-catenin, implicating it in store-operated Ca(2+) entry (SOCE). Ca(2+) release from ER stores under extracellular Ca(2+)-free conditions using thapsigargin (1 μM) to inhibit endoplasmic Ca(2+) ATPase (SERCA) followed by re-adjustment of extracellular Ca(2+) to physiological levels activated SOCE, which was insensitive to the blocker of numerous transient receptor potential channels and voltage-dependent Ca(2+) channels SKF96563 (1 μM). SOCE was augmented at 5 μM and inhibited at 75 μM by 2-aminoethoxydiphenyl borate which indicates the involvement Orai-1 channels. In confirmation, SOCE was decreased by siRNA knockdown of Orai-1 expression. SOCE amplitude was strongly reduced by siRNA knockdown of bestrophin-1 expression, which was due to neither changes in Stim-1/Orai-1 expression nor Stim-1/bestrophin-1 interaction. The amount of Ca(2+) released by SERCA inhibition was reduced after siRNA knockdown of bestrophin-1, but not of Orai-1. In conclusion we found that a proportion of bestrophin-1 is functionally localized to ER Ca(2+) stores where it influences the amount of Ca(2+) and therefore Ca(2+) signals which result from activation of Orai-1 via Stim-1.
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