Agonists of epoxyeicosatrienoic acids reduce infarct size and ameliorate cardiac dysfunction via activation of HO-1 and Wnt1 canonical pathway
| Autor: | Rita Rezzani, Komal Sodhi, Robert C. Touchon, Ellen Thompson, Peter L. Tsenovoy, Joseph I. Shapiro, Nader G. Abraham, John R. Falck, Jian Cao |
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| Rok vydání: | 2015 |
| Předmět: |
Male
Agonist medicine.medical_specialty Physiology medicine.drug_class Angiogenesis Wnt1 Wnt1 Protein Biology Epoxyeicosatrienoic acid Biochemistry Article Mice chemistry.chemical_compound Heme oxygenase-1 Myocardial infarction Fibrosis Internal medicine medicine Animals Humans Wnt Signaling Pathway Cells Cultured Pharmacology Aspartic Acid Adiponectin Wnt signaling pathway Membrane Proteins Cell Biology medicine.disease Endocrinology chemistry Eicosanoids Nicotinamide adenine dinucleotide phosphate |
| Zdroj: | Prostaglandins & Other Lipid Mediators. :76-86 |
| ISSN: | 1098-8823 |
| DOI: | 10.1016/j.prostaglandins.2015.01.002 |
| Popis: | Myocardial infarction (MI) is complicated by ventricular fibrosis and associated diastolic and systolic failure. Emerging studies implicate Wnt1 signaling in the formation of new blood vessels. Epoxyeicosatrienoic acids (EETs)-mediated up-regulation of heme oxygenase-1 (HO-1) protects against the detrimental consequences of MI in several animal models, however, the mechanism(s) by which this occurs remains unclear. The aim of this study was to examine these mechanisms in the LAD ligation animal model of post infarcted heart failure. Specifically, we sought to clarify the mechanistic basis of the interactions of the Wnt1 canonical pathway, HO-1 and associated angiogenesis. Human microvascular endothelial cells (HMECs) were exposed to anoxia and treated with the EET agonist, NUDSA, in the presence and absence of tin mesoporphyrin (SnMP). Increased capillary density, and Wnt1 and HO-1 expression occurred in cells treated with NUDSA. Anoxic HMECs treated with NUDSA and Wnt1 siRNA, exhibited decreased in the expression of β-catenin and the Wnt1 target gene, PPARδ (p |
| Databáze: | OpenAIRE |
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