Evidence map›Paper›PMID 23200275›Full record

ArticleCardiovascular pathology : the official journal of the Society for Cardiovascular Pathology

BMPER regulates cardiomyocyte size and vessel density in vivo.

Monte S Willis, Laura A Dyer, Rongqin Ren, Pamela Lockyer, Isabel Moreno-Miralles, Jonathan C Schisler, Cam Patterson

Abstract read
In one paragraph

Article in Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Bone Morphogenetic Proteins in Vascular Homeostasis and Disease.Cold Spring Harbor perspectives in biology · 2018
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Fenofibrate unexpectedly induces cardiac hypertrophy in mice lacking MuRF1.Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
    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

7 authors at 1 institution in 1 country.

Monte S WillisDepartment of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC 27599, USA.
Laura A Dyer
Rongqin Ren
Pamela Lockyer
Isabel Moreno-Miralles
Jonathan C Schisler
Cam Patterson
University of North Carolina at Chapel Hill · US

Funding

Signaling in endothelial growth & angiogenesisR01HL061656 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PI, XINCHUN · 1999 to 2017
$5.8M
Myocyte Signaling and the Response to StressR37HL065619 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PATTERSON, WINSTON C · 2010 to 2019
$3.7M
CHIP: A link between the chaperone &proteasome systemsR01GM061728 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SCHISLER, JONATHAN C. · 2001 to 2013
$3.4M
Myocyte specific regulation of metabolism and the response to biomechanical forceR01HL104129 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WILLIS, MONTE S · 2010 to 2018
$3.3M
NHLBI NIH HHS R01 HL061656NHLBI NIH HHS R01HL061656NHLBI NIH HHS R01 HL104129NHLBI NIH HHS R37 HL065619NIGMS NIH HHS R01 GM061728
6 · The paper itself

Abstract

backgroundBMPER, an orthologue of Drosophila melanogaster Crossveinless-2, is a secreted factor that regulates bone morphogenetic protein activity in endothelial cell precursors and during early cardiomyocyte differentiation. Although previously described in the heart, the role of BMPER in cardiac development and function remain unknown.

methodsBMPER-deficient hearts were phenotyped histologically and functionally using echocardiography and Doppler analysis. Since BMPER -/- mice die perinatally, adult BMPER +/- mice were challenged to pressure-overload-induced cardiac hypertrophy and hindlimb ischemia to determine changes in angiogenesis and regulation of cardiomyocyte size.

resultsWe identify for the first time the cardiac phenotype associated with BMPER haploinsufficiency. BMPER messenger RNA and protein are present in the heart during cardiac development through at least E14.5 but is lost by E18.5. BMPER +/- ventricles are thinner and less compact than sibling wild-type hearts. In the adult, BMPER +/- hearts present with decreased anterior and posterior wall thickness, decreased cardiomyocyte size and an increase in cardiac vessel density. Despite these changes, BMPER +/- mice respond to pressure-overload-induced cardiac hypertrophy challenge largely to the same extent as wild-type mice.

conclusionBMPER appears to play a role in regulating both vessel density and cardiac development in vivo; however, BMPER haploinsufficiency does not result in marked effects on cardiac function or adaptation to pressure overload hypertrophy.

Indexed as

AnimalsBlotting, WesternCardiomegalyCarrier ProteinsCell EnlargementCoronary VesselsHeartImmunohistochemistryIn Situ HybridizationMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacNeovascularization, PhysiologicOligonucleotide Array Sequence AnalysisReal-Time Polymerase Chain ReactionCarrier Proteinscrossveinless 2 protein, mouse

Identifiers

PMID23200275
PMCPMC5027882
OpenAlexW2038082996

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.