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大鼠心脏发育和应激过程中短链酰基辅酶A脱氢酶的变化

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

作者信息

Huang Jinxian, Xu Lipeng, Huang Qiuju, Luo Jiani, Liu Peiqing, Chen Shaorui, Yuan Xi, Lu Yao, Wang Ping, Zhou Sigui

机构信息

Department of Clinical Pharmacy, GuangDong Pharmaceutical University, Guangzhou, China.

Institute of New Drug Research and Guangdong Province Key Laboratory of Pharmacodynamic Constituents of Traditional Chinese Medicine, Jinan University College of Pharmacy, Guangzhou, China.

出版信息

J Cell Mol Med. 2015 Jul;19(7):1672-88. doi: 10.1111/jcmm.12541. Epub 2015 Mar 8.

DOI:10.1111/jcmm.12541
PMID:25753319
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4511364/
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.

摘要

本研究旨在探讨脂肪酸β-氧化关键酶短链酰基辅酶A脱氢酶（SCAD）在大鼠心脏发育过程中的表达情况，以及病理和生理性心肌肥大中SCAD的差异。SCAD在胎儿和新生儿心脏中的表达最低，在正常心脏发育过程中呈时间依赖性增加。相反，在不同年龄段的自发性高血压大鼠（SHR）中观察到SCAD表达显著降低。另一方面，游泳训练的大鼠发生生理性心肌肥大，而SHR发生病理性心肌肥大。两种心肌肥大在心肌脂肪酸利用方面表现出不同的SCAD变化。此外，SCAD在病理性心肌细胞肥大中表达显著降低，而在生理性心肌细胞肥大中表达增加。SCAD siRNA处理引发病理性心肌细胞肥大，这表明SCAD表达下调可能在病理性心肌肥大中起重要作用。过氧化物酶体增殖物激活受体α（PPARα）的变化与SCAD一致。此外，特异性PPARα配体非诺贝特处理增加了SCAD的表达并抑制了病理性心肌肥大。因此，我们推测病理性心肌肥大中SCAD表达下调可能是“胎儿能量代谢重现”的原因。PPARα失活可能导致病理性心肌肥大中SCAD表达降低。SCAD在病理性和生理性心肌肥大中的变化不同，这可能用作病理性和生理性心肌肥大的分子标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/5ed070876df4/jcmm0019-1672-f19.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/c010f2ba604d/jcmm0019-1672-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/c3dea3fb4221/jcmm0019-1672-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/f8b09b36454e/jcmm0019-1672-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/b32cff6e7eb7/jcmm0019-1672-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/e3a2f0d84bb6/jcmm0019-1672-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/e9ba49601ee1/jcmm0019-1672-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/2be44e4f4902/jcmm0019-1672-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/9d16bfc10b6d/jcmm0019-1672-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/ed106906b157/jcmm0019-1672-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/bab3278b0fa7/jcmm0019-1672-f10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/263e5771f657/jcmm0019-1672-f11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/d1a050bb0f2a/jcmm0019-1672-f12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/953fcbb00aba/jcmm0019-1672-f13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/6aea66e96be7/jcmm0019-1672-f14.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/ff324397c10b/jcmm0019-1672-f15.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/6914d73c823f/jcmm0019-1672-f16.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/caa3b4ac3c87/jcmm0019-1672-f17.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/dcc37ba2625d/jcmm0019-1672-f18.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/5ed070876df4/jcmm0019-1672-f19.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/c010f2ba604d/jcmm0019-1672-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/c3dea3fb4221/jcmm0019-1672-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/f8b09b36454e/jcmm0019-1672-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/b32cff6e7eb7/jcmm0019-1672-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/e3a2f0d84bb6/jcmm0019-1672-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/e9ba49601ee1/jcmm0019-1672-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/2be44e4f4902/jcmm0019-1672-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/9d16bfc10b6d/jcmm0019-1672-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/ed106906b157/jcmm0019-1672-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/bab3278b0fa7/jcmm0019-1672-f10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/263e5771f657/jcmm0019-1672-f11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/d1a050bb0f2a/jcmm0019-1672-f12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/953fcbb00aba/jcmm0019-1672-f13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/6aea66e96be7/jcmm0019-1672-f14.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/ff324397c10b/jcmm0019-1672-f15.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/6914d73c823f/jcmm0019-1672-f16.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/caa3b4ac3c87/jcmm0019-1672-f17.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/dcc37ba2625d/jcmm0019-1672-f18.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e220/4511364/5ed070876df4/jcmm0019-1672-f19.jpg

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