Evidence map›Paper›PMID 24362315›Full record

ArticleCell cycle (Georgetown, Tex.)2014

CENP-A is essential for cardiac progenitor cell proliferation.

Michael McGregor, Nirmala Hariharan, Anya Y Joyo, Robert L Margolis, Mark A Sussman

Open access · hybridAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-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

15 citing papers in PubMed, 29 citations in OpenAlex.

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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

5 authors at 3 institutions in 1 country.

Michael McGregorSan Diego Heart Research Institute and the Department of Biology; San Diego State University; San Diego, CA USA.
Nirmala HariharanSan Diego Heart Research Institute and the Department of Biology; San Diego State University; San Diego, CA USA.
Anya Y JoyoSan Diego Heart Research Institute and the Department of Biology; San Diego State University; San Diego, CA USA.
Robert L MargolisSanford-Burnham Medical Research Institute; La Jolla, CA USA.
Mark A SussmanSan Diego Heart Research Institute and the Department of Biology; San Diego State University; San Diego, CA USA.
University of California, San Diego · USLa Jolla Alcohol Research · USSan Diego State University · US

Funding

Surgery, Physiology and ImmunohistopathologyP01HL085577 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI GUSTAFSSON, ASA B. · 2006 to 2017
$18.4M
Regulation of Signal Transduction to Treat Heart FailureR01HL067245 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN · 2001 to 2021
$6.0M
Stem Cell Signaling in the Pathologically Challenged MyocardiumR37HL091102 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN · 2008 to 2017
$3.8M
Beta-adrenergic signaling: double edged sword of myocardial repairR01HL117163 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN · 2013 to 2017
$1.9M
Antagonism of myocardial aging and senescence with Pim-1 kinaseR01HL105759 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN · 2011 to 2015
$1.8M
Enhanced Myocardial Repair with CardioClusters and CardioChimerasR01HL122525 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN · 2014 to 2017
$1.5M
Cardioprotection by optimizing mTOR activityR01HL113647 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN · 2013 to 2016
$1.5M
Molecular Engineering of Damaged Myocardium To Enhance Regeneration And RepairR01HL113656 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN · 2012 to 2013
$667k
NHLBI NIH HHS 1R01HL105759NHLBI NIH HHS 1R01HL113647NHLBI NIH HHS 1R01HL113656NHLBI NIH HHS 1R01HL117163NHLBI NIH HHS 1R37HL091102NHLBI NIH HHS 5R01HL067245NHLBI NIH HHS P01 HL085577NHLBI NIH HHS R01 HL067245NHLBI NIH HHS R01 HL105759NHLBI NIH HHS R01 HL113647NHLBI NIH HHS R01 HL113656NHLBI NIH HHS R01 HL117163NHLBI NIH HHS R01 HL122525NHLBI NIH HHS R37 HL091102
6 · The paper itself

Abstract

Centromere protein A (CENP-A) is a homolog of histone H3 that epigenetically marks the heterochromatin of chromosomes. CENP-A is a critical component of the cell cycle machinery that is necessary for proper assembly of the mitotic spindle. However, the role of CENP-A in the heart and cardiac progenitor cells (CPCs) has not been previously studied. This study shows that CENP-A is expressed in CPCs and declines with age. Silencing CENP-A results in a decreased CPC growth rate, reduced cell number in phase G 2/M of the cell cycle, and increased senescence associated β-galactosidase activity. Lineage commitment is not affected by CENP-A silencing, suggesting that cell cycle arrest induced by loss of CENP-A is a consequence of senescence and not differentiation. CENP-A knockdown does not exacerbate cell death in undifferentiated CPCs, but increases apoptosis upon lineage commitment. Taken together, these results indicate that CPCs maintain relatively high levels of CENP-A early in life, which is necessary for sustaining proliferation, inhibiting senescence, and promoting survival following differentiation of CPCs.

Indexed as

Cell ProliferationAnimalsAutoantigensCell DeathCell DifferentiationCells, CulturedCell SurvivalCellular SenescenceCentromere Protein AChromosomal Proteins, Non-HistoneG2 Phase Cell Cycle CheckpointsMiceMyocardiumStem CellsAutoantigensCenpa protein, mouseCentromere Protein AChromosomal Proteins, Non-Histonecardiac progenitor cellcell cycleCENP-Aheartsenescence

Identifiers

PMID24362315
PMCPMC3979910
OpenAlexW2065825771

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.