Evidence map›Paper›PMID 15564283›Full record

ArticleThe Journal of physiology2005

Volume sensitivity of the bestrophin family of chloride channels.

Rodolphe Fischmeister, H Criss Hartzell

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.0field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

58 citing papers in PubMed, 120 citations in OpenAlex.

  1. Gene Therapy Strategies for the Treatment of Bestrophinopathies.International journal of molecular sciences · 2025
    Review
  2. The pentameric chloride channel BEST1 is activated by extracellular GABA.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Article
  5. Endogenous ion channels expressed in human embryonic kidney (HEK-293) cells.Pflugers Archiv : European journal of physiology · 2022
    Review
  6. Glial Chloride Channels in the Function of the Nervous System Across Species.Advances in experimental medicine and biology · 2021
    Article
  7. Article
  8. Disease-causing mutations associated with bestrophinopathies promote apoptosis in retinal pigment epithelium cells.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2020
    Article
  9. Article
  10. Chloride - The Underrated Ion in Nociceptors.Frontiers in neuroscience · 2020
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  18. Article
  19. Article
  20. Bestrophin 1 and retinal disease.Progress in retinal and eye research · 2017
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Rodolphe FischmeisterDepartment of Cell Biology, Emory University School of Medicine, 615 Michael Street, 535 Whitehead Biomedical Research Building, Atlanta, GA 30322-3030, USA.
H Criss Hartzell
Emory University · USLaboratoire de Génétique Cellulaire · FR

Funding

Retinal Degeneration and Chloride ChannelsR01EY014852 · NEI · EMORY UNIVERSITY · PI HARTZELL, H. CRISS · 2003 to 2020
$5.7M
REGULATION OF CALCIUM-ACTIVATED CHLORIDE CHANNELSR01GM060448 · NIGMS · EMORY UNIVERSITY · PI HARTZELL, H. CRISS · 2000 to 2014
$3.7M
NEI NIH HHS EY 014852NEI NIH HHS R01 EY014852NIGMS NIH HHS GM 60448NIGMS NIH HHS R01 GM060448
6 · The paper itself

Abstract

Bestrophins are a newly identified family of Cl(-) channels. Mutations in the founding member of the family, human bestrophin-1 (hBest1), are responsible for a form of early onset macular degeneration called Best vitelliform macular dystrophy. The link between dysfunction of hBest1 and macular degeneration remains unknown. Because retinal pigmented epithelium (RPE) cells may be subjected to varying osmotic pressure due to light-dependent changes in the ionic composition of the subretinal space and because RPE cells may undergo large volume changes during phagocytosis of shed photoreceptor discs, we investigated whether bestrophin currents were affected by cell volume. When hBest1 and mBest2 were overexpressed in HEK 293, HeLa, and ARPE-19 cells, a new Ca(2+)-activated Cl(-) current appeared. This current was very sensitive to cell volume. A 20% increase in extracellular osmolarity caused cell shrinkage and a approximately 70-80% reduction in bestrophin current. Decreases in extracellular osmolarity increased the bestrophin currents slightly, but this was difficult to quantify due to simultaneous activation of endogenous volume-regulated anion channel (VRAC) current. To determine whether a similar current was present in mouse RPE cells, the effect of hyperosmotic solutions on isolated mouse RPE cells was examined. Mouse RPE cells exhibited an endogenous Cl(-) current that resembled the expressed hBest1 in that it was decreased by hypertonic solution. We conclude that bestrophins are volume sensitive and that they could play a novel role in cell volume regulation of RPE cells.

Indexed as

AnimalsBestrophinsBiotinCell SeparationCell SizeChloride ChannelsElectrophysiologyEpithelial CellsEye ProteinsHumansImage Processing, Computer-AssistedIn Vitro TechniquesKineticsMembrane PotentialsMembrane ProteinsMiceBEST1 protein, humanBestrophinsBiotinChloride ChannelsEye ProteinsMembrane ProteinsSolutions

Identifiers

PMID15564283
PMCPMC1665509
OpenAlexW2124608352

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.