Effects of ERK1/2/PPARα/SCAD signal pathways on cardiomyocyte hypertrophy induced by insulin-like growth factor 1 and phenylephrine
| Autor: | Bing Liu, Qiuju Huang, Xuediao Pan, Linquan Zang, Zhenhua Zeng, Shaorui Chen, Peiqing Liu, Jiani Luo, Jinxian Huang, Sigui Zhou |
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| Rok vydání: | 2015 |
| Předmět: |
Butyryl-CoA Dehydrogenase
medicine.medical_specialty MAP Kinase Signaling System medicine.medical_treatment Cell Cardiomegaly Biology General Biochemistry Genetics and Molecular Biology Rats Sprague-Dawley Phenylephrine Insulin-like growth factor Fenofibrate Internal medicine medicine Animals Myocytes Cardiac PPAR alpha Insulin-Like Growth Factor I Phosphorylation General Pharmacology Toxicology and Pharmaceutics Oxazoles Beta oxidation Flavonoids chemistry.chemical_classification Activator (genetics) Fatty Acids Fatty acid General Medicine Rats Disease Models Animal medicine.anatomical_structure Endocrinology Animals Newborn chemistry Tyrosine Signal transduction Signal Transduction medicine.drug |
| Zdroj: | Life Sciences. 124:41-49 |
| ISSN: | 0024-3205 |
| Popis: | Aims Short-chain acyl-CoA dehydrogenase (SCAD) is a key enzyme in fatty acid oxidation. In the present study we aim to investigate the changes in SCAD between pathological and physiological cardiomyocyte hypertrophy. We also explore the different signaling pathways of pathological and physiological cardiomyocyte hypertrophy. Main methods After neonatal rat cardiomyocytes were treated as setups, cell surface area, expression of SCAD, PPARα, phospho-ERK1/2, activity of SCAD, free fatty acid content and ATP content in the cardiomyocytes were measured. Key findings Neonatal rat cardiomyocytes treated by PE showed an increased cell surface area and free fatty acid content, increased ERK1/2 phosphorylation, decreased expression of PPARα, decreased expression and activity of SCAD and decreased levels of ATP. Neonatal rat cardiomyocytes treated by IGF-1 showed the reverse effects except for the cell surface area. PPARα inhibitor GW6471 and PPARα activator Fenofibrate treatments abrogated the effects induced by IGF-1 and PE in cardiomyocytes respectively, as well as ERK1/2 activator EGF and ERK1/2 inhibitor PD98059. Significance SCAD has different changes between pathological and physiological cardiomyocyte hypertrophy. The ERK1/2/PPARα/SCAD signaling pathways play different roles in pathological and physiological cardiomyocyte hypertrophy. SCAD may be used as a new target to prevent the development of pathological cardiac hypertrophy. |
| Databáze: | OpenAIRE |
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