Transcriptomic analysis of left ventricle myocardium in an SHR congenic line with ameliorated cardiac fibrosis
Language English Country Czech Republic Media print-electronic
Document type Comparative Study, Journal Article
PubMed
31424260
DOI
10.33549/physiolres.934127
PII: 934127
Knihovny.cz E-resources
- MeSH
- Phenotype MeSH
- Fibrosis MeSH
- Ventricular Function, Left genetics MeSH
- Genetic Predisposition to Disease MeSH
- Hypertension genetics metabolism physiopathology MeSH
- Cardiomyopathies genetics metabolism pathology MeSH
- Blood Pressure genetics MeSH
- Metabolic Syndrome genetics metabolism physiopathology MeSH
- Disease Models, Animal MeSH
- Rats, Inbred SHR MeSH
- Gene Expression Regulation MeSH
- Ventricular Remodeling genetics MeSH
- Signal Transduction genetics MeSH
- Heart Ventricles metabolism pathology MeSH
- Gene Expression Profiling * MeSH
- Transcriptome * MeSH
- Animals, Congenic MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Comparative Study MeSH
Metabolic syndrome and one of its manifestations, essential hypertension, is an important cause of worldwide morbidity and mortality. Morbidity and mortality associated with hypertension are caused by organ complications. Previously we revealed a decrease of blood pressure and an amelioration of cardiac fibrosis in a congenic line of spontaneously hypertensive rats (SHR), in which a short segment of chromosome 8 (encompassing only 7 genes) was exchanged for a segment of normotensive polydactylous (PD) origin. To unravel the genetic background of this phenotype we compared heart transcriptomes between SHR rat males and this chromosome 8 minimal congenic line (PD5). We found 18 differentially expressed genes, which were further analyzed using annotations from Database for Annotation, Visualization and Integrated Discovery (DAVID). Four of the differentially expressed genes (Per1, Nr4a1, Nr4a3, Kcna5) belong to circadian rhythm pathways, aldosterone synthesis and secretion, PI3K-Akt signaling pathway and potassium homeostasis. We were also able to confirm Nr4a1 2.8x-fold upregulation in PD5 on protein level using Western blotting, thus suggesting a possible role of Nr4a1 in pathogenesis of the metabolic syndrome.
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