C/EBPβ knockdown protects cardiomyocytes from hypertrophy via inhibition of p65-NFκB.
C/EBPβ, a member of the bHLH gene family of DNA-binding transcription factors, has been indicated as a central signal in physiologic hypertrophy. However, the role of C/EBPβ in pathological cardiac hypertrophy remains to be elucidated. In this study, we revealed that C/EBPβ is involved in cardiac hypertrophy, the expression of C/EBPβ were significantly increased in response to hypertrophic stimulation in vitro and in vivo. C/EBPβ knockdown inhibited PE-induced cardiac hypertrophy, and diminished the nuclear translocation and DNA binding activity of p65-NFκB. These results suggested that C/EBPβ knockdown protected cardiomyocytes from hypertrophy, which may be attributed to inhibition of NFκB-dependent transcriptional activity. These findings shed new light on the understanding of C/EBPβ-related cardiomyopathy, and suggest the potential application of C/EBPβ inhibitors in cardiac hypertrophy.
Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China; Department of Pharmacy, Chengdu Fifth People's Hospital, Chengdu 611130, China.
Jian
J
Zou
Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
Hong
H
Li
Department of Pharmacy, Changsha Central Hospital, Changsha 410004, China.
Xi
X
Chen
Department of Pharmacy, Guangdong No.2 Provincial People's Hospital, Guangzhou 524000, China.
Siyu
S
Zeng
Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
Jiantao
J
Ye
Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
Changhua
C
Zhou
Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
Min
M
Liu
Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
Luankun
L
Zhang
Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
Na
N
Yu
Department of Pharmacy, Chengdu Fifth People's Hospital, Chengdu 611130, China.
Xiaohong
X
Gan
Department of Pharmacy, Chengdu Fifth People's Hospital, Chengdu 611130, China.
Houfeng
H
Zhou
Department of Pharmacy, Chengdu Fifth People's Hospital, Chengdu 611130, China.
Zhiwei
Z
Xian
Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China. Electronic address: chshaor@mail.sysu.edu.cn.
Shaorui
S
Chen
Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China. Electronic address: liupq@mail.sysu.edu.cn.
Peiqing
P
Liu
D021581:Active Transport, Cell Nucleus; D000818:Animals; D022782:CCAAT-Enhancer-Binding Protein-beta / Q000235:genetics* / Q000378:metabolism; D002478:Cells, Cultured; D004247:DNA / Q000378:metabolism; D024202:Electrophoretic Mobility Shift Assay; D015870:Gene Expression; D055785:Gene Knockdown Techniques; D006984:Hypertrophy / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D011485:Protein Binding; D017207:Rats, Sprague-Dawley; D051996:Transcription Factor RelA / Q000235:genetics / Q000378:metabolism*
D022782:CCAAT-Enhancer-Binding Protein-beta; C545014:Cebpb protein, rat; C498145:Rela protein, rat; D051996:Transcription Factor RelA; D004247:DNA
C/EBPβ; Cardiac hypertrophy; p65-NFκB