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Changes in short-chain acyl-coA dehydrogenase during rat cardiac development and stress.

Abstract
This study was designed to investigate the expression of short-chain acyl-CoA dehydrogenase (SCAD), a key enzyme of fatty acid β-oxidation, during rat heart development and the difference of SCAD between pathological and physiological cardiac hypertrophy. The expression of SCAD was lowest in the foetal and neonatal heart, which had time-dependent increase during normal heart development. In contrast, a significant decrease in SCAD expression was observed in different ages of spontaneously hypertensive rats (SHR). On the other hand, swim-trained rats developed physiological cardiac hypertrophy, whereas SHR developed pathological cardiac hypertrophy. The two kinds of cardiac hypertrophy exhibited divergent SCAD changes in myocardial fatty acids utilization. In addition, the expression of SCAD was significantly decreased in pathological cardiomyocyte hypertrophy, however, increased in physiological cardiomyocyte hypertrophy. SCAD siRNA treatment triggered the pathological cardiomyocyte hypertrophy, which showed that the down-regulation of SCAD expression may play an important role in pathological cardiac hypertrophy. The changes in peroxisome proliferator-activated receptor α (PPARα) was accordant with that of SCAD. Moreover, the specific PPARα ligand fenofibrate treatment increased the expression of SCAD and inhibited pathological cardiac hypertrophy. Therefore, we speculate that the down-regulated expression of SCAD in pathological cardiac hypertrophy may be responsible for 'the recapitulation of foetal energy metabolism'. The deactivation of PPARα may result in the decrease in SCAD expression in pathological cardiac hypertrophy. Changes in SCAD are different in pathological and physiological cardiac hypertrophy, which may be used as the molecular markers of pathological and physiological cardiac hypertrophy.
AuthorsJinxian Huang, Lipeng Xu, Qiuju Huang, Jiani Luo, Peiqing Liu, Shaorui Chen, Xi Yuan, Yao Lu, Ping Wang, Sigui Zhou
JournalJournal of cellular and molecular medicine (J Cell Mol Med) Vol. 19 Issue 7 Pg. 1672-88 (Jul 2015) ISSN: 1582-4934 [Electronic] England
PMID25753319 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Copyright© 2015 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
Chemical References
  • Fatty Acids
  • PPAR alpha
  • RNA, Messenger
  • RNA, Small Interfering
  • Phenylephrine
  • Insulin-Like Growth Factor I
  • Butyryl-CoA Dehydrogenase
  • Fenofibrate
Topics
  • Animals
  • Animals, Newborn
  • Blood Pressure (drug effects)
  • Butyryl-CoA Dehydrogenase (genetics, metabolism)
  • Cardiomegaly (diagnostic imaging, enzymology, pathology, physiopathology)
  • Disease Models, Animal
  • Fatty Acids (metabolism)
  • Fenofibrate (pharmacology)
  • Heart (drug effects, growth & development, physiopathology)
  • Heart Ventricles (pathology, physiopathology)
  • Insulin-Like Growth Factor I (pharmacology)
  • Myocytes, Cardiac (drug effects, metabolism, pathology)
  • Organ Size (drug effects)
  • Oxidation-Reduction (drug effects)
  • PPAR alpha (metabolism)
  • Phenylephrine (pharmacology)
  • RNA Interference (drug effects)
  • RNA, Messenger (genetics, metabolism)
  • RNA, Small Interfering (metabolism)
  • Rats, Inbred SHR
  • Rats, Wistar
  • Substrate Specificity (drug effects)
  • Systole (drug effects)
  • Time Factors
  • Ultrasonography

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