Evidence map›Paper›PMID 20186580›Full record

ArticleCardiovascular toxicology2010

Exposure to low-dose trichloroethylene alters shear stress gene expression and function in the developing chick heart.

Om Makwana, Nicholas M P King, Lauren Ahles, Ornella Selmin, Henk L Granzier, Raymond B Runyan

Open access · greenAbstract read
In one paragraph

Article in Cardiovascular toxicology, 2010. 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
0.4field-weighted citation impact, top 38% 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, 26 citations in OpenAlex.

  1. Review
  2. Review
  3. Mechanosensitive Pathways in Heart Development: Findings from Chick Embryo Studies.Journal of cardiovascular development and disease · 2021
    Review
  4. Review
  5. Article
  6. Article
  7. Article
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  9. Review
  10. 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

6 authors at 1 institution in 1 country.

Om MakwanaDepartment of Cell Biology and Anatomy, University of Arizona, 1501 N Campbell Avenue, PO Box 245044, Tucson, AZ 85724-5044, USA.
Nicholas M P King
Lauren Ahles
Ornella Selmin
Henk L Granzier
Raymond B Runyan
University of Arizona · US

Funding

SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI Paloma Inés Beamer · 1994 to 2026
$36.7M
Cardiovascular Biomedical Engineering Training GrantT32HL007955 · NHLBI · UNIVERSITY OF ARIZONA · PI BARTON, JENNIFER KEHLET · 2001 to 2020
$5.1M
Regulation of EMT During Avian Heart Valve FormationR01HL082851 · NHLBI · UNIVERSITY OF ARIZONA · PI RUNYAN, RAYMOND BRUCE · 2007 to 2010
$1.5M
NHLBI NIH HHS R01 HL082851NHLBI NIH HHS T32 HL007955NIEHS NIH HHS ES006694NIEHS NIH HHS P30 ES006694
6 · The paper itself

Abstract

Trichloroethylene is an organic solvent used as an industrial degreasing agent. Due to its widespread use and volatile nature, TCE is a common environmental contaminant. Trichloroethylene exposure has been implicated in the etiology of heart defects in human populations and animal models. Recent data suggest misregulation of Ca2+ homeostasis in H9c2 cardiomyocyte cell line after TCE exposure. We hypothesized that misregulation of Ca2+ homeostasis alters myocyte function and leads to changes in embryonic blood flow. In turn, changes in cardiac flow are known to cause cardiac malformations. To investigate this hypothesis, we dosed developing chick embryos in ovo with environmentally relevant doses of TCE (8 and 800 ppb). RNA was isolated from control and treated embryos at specific times in development for real-time PCR analysis of blood flow markers. Effects were observed on Endothelin-1 (ET-1), Nitric Oxide Synthase-3 (NOS-3) and Krüppel-like Factor 2 (KLF2) expression relative to TCE exposure and consistent with reduced flow. Further, we measured function in the developing heart after TCE exposure by isolating cardiomyocytes and measuring half-width of contraction and sarcomere lengths. These functional data showed a significant increase in half-width of contraction after TCE exposure. These data suggest that perturbation of cardiac function contributes to the etiology of congenital heart defects in TCE-exposed embryos.

Indexed as

AnimalsBiomarkersBlood Flow VelocityChick EmbryoDose-Response Relationship, DrugEmbryo, NonmammalianEndothelin-1Gene ExpressionHeartKruppel-Like Transcription FactorsMyocytes, CardiacNitric Oxide Synthase Type IIISolventsStress, MechanicalTeratogensTrichloroethyleneBiomarkersEndothelin-1Kruppel-Like Transcription FactorsNitric Oxide Synthase Type IIISolventsTeratogensTrichloroethylene

Identifiers

PMID20186580
PMCPMC3069695
OpenAlexW1996807311

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.