ArticleToxicological sciences : an official journal of the Society of Toxicology2008
Trichloroethylene disrupts cardiac gene expression and calcium homeostasis in rat myocytes.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 29 citations in OpenAlex.
- Wnt 5a mediated inflammatory injury of renal tubular epithelial cells dependent on calcium signaling pathway in Trichloroethylene sensitized mice.Ecotoxicology and environmental safety · 2022Article
- HNF4a transcription is a target of trichloroethylene toxicity in the embryonic mouse heart.Environmental science. Processes & impacts · 2020Article
- Trichloroethylene perturbs HNF4a expression and activity in the developing chick heart.Toxicology letters · 2018Article
- A systematic evaluation of the potential effects of trichloroethylene exposure on cardiac development.Reproductive toxicology (Elmsford, N.Y.) · 2016Review
- Human health effects of trichloroethylene: key findings and scientific issues.Environmental health perspectives · 2013Review
- Low-dose trichloroethylene alters cytochrome P450-2C subfamily expression in the developing chick heart.Cardiovascular toxicology · 2013Article
- Adjuvant arthritis influences expression of housekeeping genes.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2011Article
- Exposure to low-dose trichloroethylene alters shear stress gene expression and function in the developing chick heart.Cardiovascular toxicology · 2010Article
- Gene expression profiling in the fetal cardiac tissue after folate and low-dose trichloroethylene exposure.Birth defects research. Part A, Clinical and molecular teratology · 2010Article
- Altered cardiac function and ventricular septal defect in avian embryos exposed to low-dose trichloroethylene.Toxicological sciences : an official journal of the Society of Toxicology · 2010Article
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6 authors at 2 institutions in 1 country.
Funding
Abstract
We have been investigating the molecular mechanisms by which trichloroethylene (TCE) might induce cardiac malformations in the embryonic heart. Previous results indicated that TCE disrupted expression of genes encoding proteins involved in regulation of intracellular Ca2+, [Ca2+](i), in cardiac cells, including ryanodine receptor isoform 2 (Ryr2), and sarcoendoplasmatic reticulum Ca2+ ATPase, Serca2a. These observations are important in light of the notion that altered cardiac contractility can produce morphological defects. The hypothesis tested in this study is that the TCE-induced changes in gene expression of Ca2+-associated proteins resulted in altered Ca2+ flux regulation. We used real-time PCR and digital imaging microscopy to characterize effects of various doses of TCE on gene expression and Ca2+ response to vasopressin (VP) in rat cardiac H9c2 myocytes. We observed a reduction in Serca2a and Ryr2 expression at 12 and 48 h after exposure to TCE. In addition, we found significant differences in Ca2+ response to VP in cells treated with TCE doses as low as 10 parts per billion. Taken all together, our data strongly indicate that exposure to TCE disrupts the ability of myocytes to regulate cellular Ca2+ fluxes. Perturbation of calcium signaling alters cardiac cell physiology and signal transduction and may hint to morphogenetic consequences in the context of heart development. These results point to a novel area of TCE biology and, if confirmed in vivo, may help to explain the apparent cardio-specific toxicity of TCE exposure in the rodent embryo.
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