ArticleStress (Amsterdam, Netherlands)2020
Myocardial fibrosis, inflammation, and altered cardiac gene expression profiles in rats exposed to a predator-based model of posttraumatic stress disorder.
Article in Stress (Amsterdam, Netherlands), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- Unraveling Complex Interactions Mechanisms Linking PTSD and Chronic Diseases.Current neuropharmacology · 2026Review
- Cathepsin S activity controls chronic stress-induced muscle atrophy and dysfunction in mice.Cellular and molecular life sciences : CMLS · 2023Article
- Dog ownership may promote cardiometabolic health in U.S. military veterans.Scientific reports · 2023Article
- Pro-arrhythmic role of adrenergic spatial densities in the human atria: An in-silico study.PloS one · 2023Article
- Berberine alleviates myocardial ischemia-reperfusion injury by inhibiting inflammatory response and oxidative stress: the key function of miR-26b-5p-mediated PTGS2/MAPK signal transduction.Pharmaceutical biology · 2022Article
- Methamphetamine-induced changes in myocardial gene transcription are sex-dependent.BMC genomics · 2021Article
- TLR4/MyD88/NF-κB-Mediated Inflammation Contributes to Cardiac Dysfunction in Rats of PTSD.Cellular and molecular neurobiology · 2020Article
- Expression and clinical significance of NRLP1 in patients with ST-segment elevation myocardial infarction combined with malignant ventricular arrhythmia.Pakistan journal of medical sciencesArticle
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Authors and funding
12 authors at 3 institutions in 1 country.
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Abstract
People who are exposed to life-threatening trauma are at risk of developing posttraumatic stress disorder (PTSD). In addition to psychological manifestations, PTSD is associated with an increased risk of myocardial infarction, arrhythmias, hypertension, and other cardiovascular problems. We previously reported that rats exposed to a predator-based model of PTSD develop myocardial hypersensitivity to ischemic injury. This study characterized cardiac changes in histology and gene expression in rats exposed this model. Male rats were subjected to two cat exposures (separated by a period of 10 d) and daily cage-mate changes for 31 d. Control rats were not exposed to the cat or cage-mate changes. Ventricular tissue was analyzed by RNA sequencing, western blotting, histology, and immunohistochemistry. Multifocal lesions characterized by necrosis, mononuclear cell infiltration, and collagen deposition were observed in hearts from all stressed rats but none of the control rats. Gene expression analysis identified clusters of upregulated genes associated with endothelial to mesenchymal transition, endothelial migration, mesenchyme differentiation, and extracellular matrix remodeling in hearts from stressed rats. Consistent with endothelial to mesenchymal transition, rats from stressed hearts exhibited increased expression of α-smooth muscle actin (a myofibroblast marker) and a decrease in the number of CD31 positive endothelial cells. These data provide evidence that predator-based stress induces myocardial lesions and reprograming of cardiac gene expression. These changes may underlie the myocardial hypersensitivity to ischemia observed in these animals. This rat model may provide a useful tool for investigating the cardiac impact of PTSD and other forms of chronic psychological stress.
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