scholarly journals Role of peroxisome proliferator-activated receptor alpha in the expression of hepatic fatty acid oxidation-related genes in chickens

2015 ◽  
Vol 87 (1) ◽  
pp. 61-66 ◽  
Author(s):  
Kazuhisa Honda ◽  
Takaoki Saneyasu ◽  
Haruka Sugimoto ◽  
Kiyotaka Kurachi ◽  
Shoko Takagi ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Receptor Alpha ◽  
Hepatic Fatty Acid ◽  
Hepatic Fatty Acid Oxidation

scholarly journals Cyclin D1 represses peroxisome proliferator-activated receptor alpha and inhibits fatty acid oxidation

Oncotarget ◽  
2016 ◽  
Vol 7 (30) ◽  
pp. 47674-47686 ◽  
Author(s):  
Sushama Kamarajugadda ◽  
Jennifer R. Becker ◽  
Eric A. Hanse ◽  
Douglas G. Mashek ◽  
Mara T. Mashek ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Cyclin D1 ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Receptor Alpha

scholarly journals The role of angiopoietin-like protein 4 in phenylephrine-induced cardiomyocyte hypertrophy

2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Yu Sun ◽  
Yi Li ◽  
Chen Liu ◽  
Ruicong Xue ◽  
Bin Dong ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Cell Surface ◽  
Fatty Acid Oxidation ◽  
Cardiomyocyte Hypertrophy ◽  
Acid Oxidation ◽  
Peroxisome Proliferator ◽  
Secreted Protein ◽  
Peroxisome Proliferator Activated Receptor ◽  
Regulated Expression

Abstract Angiopoietin-like protein 4 (ANGPTL4) is a multifunctional secreted protein that can be induced by fasting, hypoxia and glucocorticoids. ANGPTL4 has been associated with a variety of diseases; however, the role of ANGPTL4 in cardiac hypertrophy remains poorly understood. In our study, we aimed to explore the effect of ANGPTL4 on phenylephrine-induced cardiomyocyte hypertrophy. Our results showed that knockdown of ANGPTL4 expression significantly exacerbated cardiomyocyte hypertrophy, as demonstrated by increased hypertrophic marker expression, including ANP and cell surface area. Moreover, significantly reduced fatty acid oxidation, as featured by decreased CPT-1 levels, was observed in hypertrophic cardiomyocytes following ANGPTL4 down-regulation. Furthermore, knockdown of ANGPLT4 led to down-regulated expression of peroxisome proliferator-activated receptor α (PPARα), which is the key regulator of cardiac fatty acid oxidation. In addition, ANGPTL4 silencing promoted the activation of JNK1/2, and JNK1/2 signaling blockade could restore the level of PPARα and significantly ameliorate the ANGPTL4 knockdown-induced cardiomyocyte hypertrophy. Therefore, our study demonstrated that ANGPTL4 regulates PPARα through JNK1/2 signaling and is required for the inhibition of cardiomyocyte hypertrophy.

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