title: 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.
authors.affiliation: Department of Clinical Pharmacy, GuangDong Pharmaceutical University, Guangzhou, China.
authors.forename: Jinxian
authors.initials: J
authors.lastname: Huang
authors.affiliation: Institute of New Drug Research and Guangdong Province Key Laboratory of Pharmacodynamic Constituents of Traditional Chinese Medicine, Jinan University College of Pharmacy, Guangzhou, China.
authors.forename: Lipeng
authors.initials: L
authors.lastname: Xu
authors.affiliation: Department of Clinical Pharmacy, GuangDong Pharmaceutical University, Guangzhou, China.
authors.forename: Qiuju
authors.initials: Q
authors.lastname: Huang
authors.affiliation: Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China.
authors.forename: Jiani
authors.initials: J
authors.lastname: Luo
authors.affiliation: Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China.
authors.forename: Peiqing
authors.initials: P
authors.lastname: Liu
authors.affiliation: Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China.
authors.forename: Shaorui
authors.initials: S
authors.lastname: Chen
authors.affiliation: Clinical Medicine Eight Years 1st Class 2007 Grade, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
authors.forename: Xi
authors.initials: X
authors.lastname: Yuan
authors.affiliation: Clinical Medicine Eight Years 1st Class 2007 Grade, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
authors.forename: Yao
authors.initials: Y
authors.lastname: Lu
authors.affiliation: Shenzhen Institute for Drug Control, Shenzhen, China.
authors.forename: Ping
authors.initials: P
authors.lastname: Wang
authors.affiliation: Department of Clinical Pharmacy, GuangDong Pharmaceutical University, Guangzhou, China.
authors.forename: Sigui
authors.initials: S
authors.lastname: Zhou
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001794:Blood Pressure / Q000187:drug effects; D044926:Butyryl-CoA Dehydrogenase / Q000235:genetics / Q000378:metabolism*; D006332:Cardiomegaly / Q000000981:diagnostic imaging / Q000201:enzymology* / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D005227:Fatty Acids / Q000378:metabolism; D011345:Fenofibrate / Q000494:pharmacology; D006321:Heart / Q000187:drug effects / Q000254:growth & development* / Q000503:physiopathology; D006352:Heart Ventricles / Q000473:pathology / Q000503:physiopathology; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D009929:Organ Size / Q000187:drug effects; D010084:Oxidation-Reduction / Q000187:drug effects; D047493:PPAR alpha / Q000378:metabolism; D010656:Phenylephrine / Q000494:pharmacology; D034622:RNA Interference / Q000187:drug effects; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D034741:RNA, Small Interfering / Q000378:metabolism; D011918:Rats, Inbred SHR; D017208:Rats, Wistar; D013379:Substrate Specificity / Q000187:drug effects; D013599:Systole / Q000187:drug effects; D013997:Time Factors; D014463:Ultrasonography
chemical_list: D005227:Fatty Acids; D047493:PPAR alpha; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D010656:Phenylephrine; D007334:Insulin-Like Growth Factor I; D044926:Butyryl-CoA Dehydrogenase; D011345:Fenofibrate
keywords: heart development; pathological cardiac hypertrophy; peroxisome proliferator-activated receptor α; physiological cardiac hypertrophy; short-chain acyl-CoA dehydrogenase