Evidence map›Paper›PMID 27404273›Full record

ArticlePloS one2016

Measurement of the Absolute Magnitude and Time Courses of Mitochondrial Membrane Potential in Primary and Clonal Pancreatic Beta-Cells.

Akos A Gerencser, Shona A Mookerjee, Martin Jastroch, Martin D Brand

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Mitochondrial responses to intracellular CaJournal of neurophysiology · 2023
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Quantitative analysis of mitochondrial membrane potential heterogeneity in unsynchronized and synchronized cancer cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. International journal of molecular sciences · 2019
    Article
  16. Review
  17. Article
  18. Mitochondrial Heterogeneity.Frontiers in genetics · 2018
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Akos A GerencserBuck Institute for Research on Aging, Novato, California, United States of America.
Shona A MookerjeeBuck Institute for Research on Aging, Novato, California, United States of America.
Martin JastrochBuck Institute for Research on Aging, Novato, California, United States of America.
Martin D BrandBuck Institute for Research on Aging, Novato, California, United States of America.
Buck Institute for Research on Aging · USMarin Community Foundation · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this study was to simplify, improve and validate quantitative measurement of the mitochondrial membrane potential (ΔψM) in pancreatic β-cells. This built on our previously introduced calculation of the absolute magnitude of ΔψM in intact cells, using time-lapse imaging of the non-quench mode fluorescence of tetramethylrhodamine methyl ester and a bis-oxonol plasma membrane potential (ΔψP) indicator. ΔψM is a central mediator of glucose-stimulated insulin secretion in pancreatic β-cells. ΔψM is at the crossroads of cellular energy production and demand, therefore precise assay of its magnitude is a valuable tool to study how these processes interplay in insulin secretion. Dispersed islet cell cultures allowed cell type-specific, single-cell observations of cell-to-cell heterogeneity of ΔψM and ΔψP. Glucose addition caused hyperpolarization of ΔψM and depolarization of ΔψP. The hyperpolarization was a monophasic step increase, even in cells where the ΔψP depolarization was biphasic. The biphasic response of ΔψP was associated with a larger hyperpolarization of ΔψM than the monophasic response. Analysis of the relationships between ΔψP and ΔψM revealed that primary dispersed β-cells responded to glucose heterogeneously, driven by variable activation of energy metabolism. Sensitivity analysis of the calibration was consistent with β-cells having substantial cell-to-cell variations in amounts of mitochondria, and this was predicted not to impair the accuracy of determinations of relative changes in ΔψM and ΔψP. Finally, we demonstrate a significant problem with using an alternative ΔψM probe, rhodamine 123. In glucose-stimulated and oligomycin-inhibited β-cells the principles of the rhodamine 123 assay were breached, resulting in misleading conclusions.

Indexed as

Membrane Potential, MitochondrialAnimalsCalibrationCell Line, TumorCell SizeClone CellsGlucoseHumansInsulin-Secreting CellsMaleOligomycinsOptical ImagingOrganometallic CompoundsPotentiometryRatsRats, WistarGlucoseOligomycinsOrganometallic Compoundstetramethyl rhodamine ethyl ester

Identifiers

PMID27404273
PMCPMC4942067
OpenAlexW2460775299

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.