Evidence map›Paper›PMID 27499046›Full record

ArticleScientific reports2016

Blunted apoptosis of erythrocytes in mice deficient in the heterotrimeric G-protein subunit Gαi2.

Rosi Bissinger, Elisabeth Lang, Mehrdad Ghashghaeinia, Yogesh Singh, Christine Zelenak, Birgit Fehrenbacher, Sabina Honisch, Hong Chen, Hajar Fakhri, Anja T Umbach and 9 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

1 citing paper in PubMed, 21 citations in OpenAlex.

  1. Heterotrimeric G-protein subunit GαPhysiological reports · 2018
    Article
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

19 authors at 6 institutions in 4 countries.

Rosi BissingerInstitute of Cardiology, Vascular Medicine and Physiology, University of Tuebingen, Germany.
Elisabeth LangDepartment of Gastroenterology, Hepatology and Infectious Diseases, University of Duesseldorf, Germany.
Mehrdad GhashghaeiniaInstitute of Cardiology, Vascular Medicine and Physiology, University of Tuebingen, Germany.
Yogesh SinghInstitute of Cardiology, Vascular Medicine and Physiology, University of Tuebingen, Germany.
Christine ZelenakDepartment of Internal Medicine, Charité Medical University, Berlin, Germany.
Birgit FehrenbacherDepartment of Dermatology, University of Tuebingen, Germany.
Sabina HonischInstitute of Cardiology, Vascular Medicine and Physiology, University of Tuebingen, Germany.
Hong ChenInstitute of Cardiology, Vascular Medicine and Physiology, University of Tuebingen, Germany.
Hajar FakhriInstitute of Cardiology, Vascular Medicine and Physiology, University of Tuebingen, Germany.
Anja T UmbachInstitute of Cardiology, Vascular Medicine and Physiology, University of Tuebingen, Germany.
Guilai LiuInstitute of Cardiology, Vascular Medicine and Physiology, University of Tuebingen, Germany.
Rexhep RexhepajInstitute of Cardiology, Vascular Medicine and Physiology, University of Tuebingen, Germany.
Guoxing LiuInstitute of Cardiology, Vascular Medicine and Physiology, University of Tuebingen, Germany.
Martin SchallerDepartment of Dermatology, University of Tuebingen, Germany.
Andreas F MackInstitute of Anatomy, University of Tuebingen, Germany.
Adrian LupescuInstitute of Cardiology, Vascular Medicine and Physiology, University of Tuebingen, Germany.
Lutz BirnbaumerNeurobiology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, Durham, NC, USA.
Florian LangInstitute of Cardiology, Vascular Medicine and Physiology, University of Tuebingen, Germany.
Syed M QadriInstitute of Cardiology, Vascular Medicine and Physiology, University of Tuebingen, Germany.
University of Tübingen · DECharité - Universitätsmedizin Berlin · DEHeinrich Heine University Düsseldorf · DENational Institute of Environmental Health Sciences · USPontificia Universidad Católica Argentina · ARUniversity of Bonn · DE

Funding

Transmembrane Signaling MechanismsZ01ES101643 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BIRNBAUMER, LUTZ · 2003 to 2008
$5.1M
Intramural NIH HHS Z01 ES101643
6 · The paper itself

Abstract

Putative functions of the heterotrimeric G-protein subunit Gαi2-dependent signaling include ion channel regulation, cell differentiation, proliferation and apoptosis. Erythrocytes may, similar to apoptosis of nucleated cells, undergo eryptosis, characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine (PS) exposure. Eryptosis may be triggered by increased cytosolic Ca(2+) activity and ceramide. In the present study, we show that Gαi2 is expressed in both murine and human erythrocytes and further examined the survival of erythrocytes drawn from Gαi2-deficient mice (Gαi2(-/-)) and corresponding wild-type mice (Gαi2(+/+)). Our data show that plasma erythropoietin levels, erythrocyte maturation markers, erythrocyte counts, hematocrit and hemoglobin concentration were similar in Gαi2(-/-) and Gαi2(+/+) mice but the mean corpuscular volume was significantly larger in Gαi2(-/-) mice. Spontaneous PS exposure of circulating Gαi2(-/-) erythrocytes was significantly lower than that of circulating Gαi2(+/+) erythrocytes. PS exposure was significantly lower in Gαi2(-/-) than in Gαi2(+/+) erythrocytes following ex vivo exposure to hyperosmotic shock, bacterial sphingomyelinase or C6 ceramide. Erythrocyte Gαi2 deficiency further attenuated hyperosmotic shock-induced increase of cytosolic Ca(2+) activity and cell shrinkage. Moreover, Gαi2(-/-) erythrocytes were more resistant to osmosensitive hemolysis as compared to Gαi2(+/+) erythrocytes. In conclusion, Gαi2 deficiency in erythrocytes confers partial protection against suicidal cell death.

Indexed as

EryptosisAnimalsCell SurvivalErythrocyte IndicesErythrocytesGTP-Binding Protein alpha Subunit, Gi2HumansMiceMice, KnockoutPhosphatidylserinesGTP-Binding Protein alpha Subunit, Gi2Phosphatidylserines

Identifiers

PMID27499046
PMCPMC4976336
OpenAlexW2483692171

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.