Muscle-specific programmed cell death 5 deletion attenuates cardiac aging

Author(s):  
Amber Naz ◽  
Shasha Zhang ◽  
Lin An ◽  
Zongpei Song ◽  
Zhenguo Zi ◽  
...  
2009 ◽  
Vol 486 (2) ◽  
pp. 141-149 ◽  
Author(s):  
Hongwei Yao ◽  
Lanjun Xu ◽  
Yingang Feng ◽  
Dongsheng Liu ◽  
Yingyu Chen ◽  
...  

2006 ◽  
Vol 30 (9) ◽  
pp. 1159-1165 ◽  
Author(s):  
Guo-Rui Ruan ◽  
Ya-Zhen Qin ◽  
Shan-Shan Chen ◽  
Jin-Lan Li ◽  
Xi Ma ◽  
...  

2018 ◽  
Vol 115 (18) ◽  
pp. 4672-4677 ◽  
Author(s):  
Seung-Hyun Lee ◽  
Jaesung Seo ◽  
Soo-Yeon Park ◽  
Mi-Hyeon Jeong ◽  
Hyo-Kyoung Choi ◽  
...  

Programmed cell death 5 (PDCD5) has been associated with human cancers as a regulator of cell death; however, the role of PDCD5 in the endothelium has not been revealed. Thus, we investigated whether PDCD5 regulates protein kinase B (PKB/AKT)-endothelial nitric oxide synthase (eNOS)–dependent signal transduction in the endothelium and affects atherosclerosis. Endothelial-specific PDCD5 knockout mice showed significantly reduced vascular remodeling compared with wild-type (WT) mice after partial carotid ligation. WT PDCD5 competitively inhibited interaction between histone deacetylase 3 (HDAC3) and AKT, but PDCD5L6R, an HDAC3-binding–deficient mutant, did not. Knockdown of PDCD5 accelerated HDAC3–AKT interaction, AKT and eNOS phosphorylation, and nitric oxide (NO) production in human umbilical vein endothelial cells. Moreover, we found that serum PDCD5 levels reflect endothelial NO production and are correlated with diabetes mellitus, high-density lipoprotein cholesterol, and coronary calcium in human samples obtained from the cardiovascular high-risk cohort. Therefore, we conclude that PDCD5 is associated with endothelial dysfunction and may be a novel therapeutic target in atherosclerosis.


Life Sciences ◽  
2013 ◽  
Vol 92 (24-26) ◽  
pp. 1208-1214 ◽  
Author(s):  
Yanhui Li ◽  
Gang Zhou ◽  
Lijun La ◽  
Xiaochun Chi ◽  
Ye Cao ◽  
...  

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