Evidence map›Paper›PMID 31914671›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020

Insulin receptor preserves mitochondrial function by binding VDAC1 in insulin insensitive mucosal epithelial cells.

Rossella Titone, Danielle M Robertson

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. IGFBP-3 functions as a molecular switch that mediates mitochondrial and metabolic homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  12. Article
  13. 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 1 institution in 1 country.

Rossella TitoneDepartment of Ophthalmology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Danielle M RobertsonDepartment of Ophthalmology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
The University of Texas Southwestern Medical Center · US

Funding

Stem Cell, Organoid and Cell Phenotyping ModuleP30EY030413 · NEI · UT SOUTHWESTERN MEDICAL CENTER · PI W MATTHEW PETROLL · 2019 to 2026
$5.9M
Effects of Systemic Disease on Corneal Epithelial PathophysiologyR01EY024546 · NEI · UT SOUTHWESTERN MEDICAL CENTER · PI DANIELLE M. ROBERTSON · 2015 to 2026
$4.3M
The role of exosomes in Pseudomonas Aeruginosa Corneal InfectionR01EY029258 · NEI · UT SOUTHWESTERN MEDICAL CENTER · PI ROBERTSON, DANIELLE M. · 2019 to 2023
$1.6M
TEM for UT Southwestern Electron Microscopy Core FacilityS10OD021685 · OD · UT SOUTHWESTERN MEDICAL CENTER · PI LUBY-PHELPS, KATHERINE J · 2017 to 2017
$398k
NEI NIH HHS P30 EY030413NEI NIH HHS R01 EY024546NEI NIH HHS R01 EY029258NIH HHS S10 OD021685
6 · The paper itself

Abstract

Unlike many epithelial tissues, the corneal epithelium is insulin insensitive, meaning it does not require insulin for glucose uptake. In this study, we show that insulin differentially regulates mitochondrial respiration in two human mucosal epithelial cell types: insulin-insensitive corneal epithelial cells and insulin-sensitive bronchial epithelial cells. In both cell types, insulin blocks glycogen synthase kinase beta (GSK3β) activity. In the corneal epithelium however, insulin selectively regulates PTEN-induced kinase 1 (PINK-1)-mediated mitophagy and mitochondrial accumulation of insulin receptor (INSR). While insulin blocked basal levels of PINK-1-mediated mitophagy in bronchial epithelial cells, mitochondrial trafficking of INSR was not detectable. We further show that in corneal epithelia, INSR interacts with the voltage-dependent anion channel-1 (VDAC1) in mitochondria and that INSR knockdown triggers robust mitochondrial fragmentation, alterations in mitochondrial polarization, and blocks the induction of PINK-1-mediated mitophagy. Collectively, these data demonstrate that INSR interacts with VDAC1 to mediate mitochondrial stability. We also demonstrate unique interactions between VDAC1 and other receptor tyrosine kinases, indicating a novel role for this family of receptors in mitochondria.

Indexed as

Antigens, CDApoptosisBiological TransportEpithelial CellsEpithelium, CornealHumansInsulinMitochondriaReceptor, InsulinVoltage-Dependent Anion Channel 1Antigens, CDINSR protein, humanInsulinReceptor, InsulinVDAC1 protein, humanVoltage-Dependent Anion Channel 1bronchial epithelial cellscorneal epithelial cellsinsulinmitochondriareceptor tyrosine kinasesVDAC1

Identifiers

PMID31914671
PMCPMC7346881
OpenAlexW2991185765

What OpenQuestion holds

Textmetadata
LicenceTDM
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.