Effects of ERK1/2/PPARα/SCAD signal pathways on physiological car-diac hypertrophy and pathological cardiac hypertrophy
10.3969/j.issn.1000-4718.2014.08.016
- VernacularTitle:ERK1／2／PPARα／SCAD 信号途径对生理性和病理性心肌肥大的调控
- Author:
Qiuju HUANG
;
Jinxian HUANG
;
Jiani LUO
;
Peiqing LIU
;
Shaorui CHEN
;
Xuediao PAN
;
Linquan ZANG
;
Sigui ZHOU
- Publication Type:Journal Article
- Keywords:
Cardiac hypertrophy;
Short-chainacyl-CoA dehydrogenase;
Extracellular signal-regulated kinase 1/2;
Peroxisome proliferator-activated receptor α;
Fatty acid oxidation
- From:
Chinese Journal of Pathophysiology
2014;(8):1427-1432
- CountryChina
- Language:Chinese
-
Abstract:
[ABSTRACT]AIM:ToinvestigatethedifferenteffectsofERK1/2/PPARα/SCAD(short-chainacyl-CoAdehy-drogenase) signal pathways on the cardiac hypertrophy induced by insulin-like growth factors 1 ( IGF-1) or phenylephrine ( PE) .METHODS:The neonatal rat cardiomyocytes induced by IGF-1 were used as the model of physiological cardiac hypertrophy , and those induced by PE were used as the model of pathological cardiac hypertrophy .The surface area of the cardiomyocytes, the expression of p-ERK1/2, PPARαand SCAD, the activity of SCAD and the content of free fatty acid in the cardiomyocytes were measured .RESULTS:Compared with the control cells , the surface area of the cardiomyocytes in-duced by IGF-1 and PE were both increased .Compared with the controls , the expression of SCAD and PPARα, and the activity of SCAD in the cardiomyocytes induced by IGF-1 were increased , while the expression of p-ERK1/2 was de-creased.However, the cardiomyocytes treated with PE showed decreased expression of SCAD and PPARα, decreased activ-ity of SCAD and increased expression of p-ERK1/2.Meanwhile, the decrease in free fatty acid in IGF-1-induced cardio-myocytes and the increase in PE-induced cardiomyocytes indicated that the fatty acid utilization was increased in the cardio -myocytes induced by IGF-1, but decreased in the cardiomyocytes induced by PE .CONCLUSION: The changes of p-ERK1/2, PPARαand SCAD in the cardiac hypertrophy induced by IGF-1 or PE indicate that the effects of ERK 1/2/PPARα/SCAD signal pathways are different between physiological cardiac hypertrophy and pathological cardiac hypertro -phy , and that SCAD may be a molecular marker of these 2 different cardiac hypertrophies and a potential therapeutic target for pathological cardiac hypertrophy .
