Evidence map›Paper›PMID 15672834›Full record

ArticleTransgenic research2004

Transgenic overexpression of cardiac actin in the mouse heart suggests coregulation of cardiac, skeletal and vascular actin expression.

A Kumar, K Crawford, R Flick, R Klevitsky, J N Lorenz, K E Bove, J Robbins, J L Lessard

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Transgenic research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.2field-weighted citation impact, top 40% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Context-dependent functional substitution of alpha-skeletal actin by gamma-cytoplasmic actin.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009
    Article
  11. 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

8 authors at 2 institutions in 1 country.

A KumarDivision of Developmental Biology, University of Cincinnati, College of Medicine, Cincinnati, OH 45229, USA. kumaa0@chmcc.org
K Crawford
R Flick
R Klevitsky
J N Lorenz
K E Bove
J Robbins
J L Lessard
University of Cincinnati Medical Center · USCincinnati Children's Hospital Medical Center · US

Funding

TARGETED ALTERATION OF ACTIN IN THE HEARTR01HL057291 · NHLBI · CHILDREN'S HOSPITAL MED CTR (CINCINNATI) · PI LESSARD, JAMES LOUIS · 1997 to 2005
$1.8M
NHLBI NIH HHS HL 57291
6 · The paper itself

Abstract

Previous studies have shown that depletion of cardiac actin by targeted disruption is associated with increased expression of alternative actins in the mouse heart. Here we have studied the effects of transgenic overexpression of cardiac actin using the alpha-myosin heavy chain promoter. Lines carrying 7 or 8 copies of the transgene showed a 2-fold increase in cardiac actin mRNA and also displayed decreased expression of skeletal and vascular actin in their hearts. In contrast, a line with more than 250 copies of the transgene did not show a similar decrease in the expression of skeletal and vascular actin despite a 3-fold increase in cardiac actin mRNA. While the low copy number transgenic mice displayed hearts that were similar to non-transgenic controls, the high copy number transgenic line showed larger hearts with distinct atrial enlargement and cardiomyocyte hypertrophy. Further, while the low copy number transgenic mouse hearts were mildly hypocontractile when compared with non-transgenic mouse hearts, the high copy number transgenic mouse hearts were significantly so. We conclude that in the presence of a small number of copies of the cardiac actin transgene, homeostatic mechanisms involved in maintaining actin levels are active and negatively regulate skeletal and vascular actin levels in the heart in response to increased expression of cardiac actin. However, these putative mechanisms are either inoperative in the high copy number transgenic line or are countered by the enhanced expression of skeletal and vascular actin during cardiomyocyte hypertrophy.

Indexed as

Gene Expression RegulationActinsAnimalsCardiomegalyGene DosageMiceMice, TransgenicMuscle, SkeletalMyocardial ContractionMyocardiumMyosin Heavy ChainsOrgan SizePromoter Regions, GeneticRNA, MessengerActinsMyosin Heavy ChainsRNA, Messenger

Identifiers

PMID15672834
OpenAlexW2057055116

What OpenQuestion holds

Textmetadata
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.