E4BP4 inhibits AngII-induced apoptosis in H9c2 cardiomyoblasts by activating the PI3K-Akt pathway and promoting calcium uptake

Bih Cheng Chen; Marthandam Asokan Shibu; Chia Hua Kuo; Chia Yao Shen; Shu Nu Chang-Lee; Chao Hung Lai; Ray Jade Chen; Chun Hsu Yao; Vijaya Padma Viswanadha; Jian Shen Liu; Wei Kung Chen; Chih Yang Huang

doi:10.1016/j.yexcr.2018.01.012

E4BP4 inhibits AngII-induced apoptosis in H9c2 cardiomyoblasts by activating the PI3K-Akt pathway and promoting calcium uptake

Bih Cheng Chen, Marthandam Asokan Shibu, Chia Hua Kuo, Chia Yao Shen, Shu Nu Chang-Lee, Chao Hung Lai, Ray Jade Chen, Chun Hsu Yao, Vijaya Padma Viswanadha, Jian Shen Liu, Wei Kung Chen, Chih Yang Huang

Research output: Contribution to journal › Article › peer-review

8 Citations (Scopus)

Abstract

The bZIP transcription factor E4BP4 is a survival factor that is known to be elevated in diseased heart and promote cell survival. In this study the role of E4BP4 on angiotensin-II (AngII)-induced apoptosis has been examined in in vitro cell model. H9c2 cardiomyoblast cells that overexpressed E4BP4 were exposed to AngII to observe the cardio-protective effects of E4BP4 on hypertension related apoptosis. The results from TUNEL assays revealed that E4BP4 significantly attenuated AngII-induced apoptosis. Further analysis by Western blot and RT-PCR showed that E4BP4 inhibited AngII-induced IGF-II mRNA expression and cleavage of caspase-3 through the PI3K-Akt pathway. In addition, E4BP4 enhanced calcium reuptake into the sacroplasmic reticulum by down-regulating PP2A and by up-regulating the phosphorylation of PKA and PLB proteins. Our findings indicate that E4BP4 functions as a survival factor in cardiomyoblasts by inhibiting IGF-II transcription and by regulating calcium cycling.

Original language	English
Pages (from-to)	227-234
Number of pages	8
Journal	Experimental Cell Research
Volume	363
Issue number	2
DOIs	https://doi.org/10.1016/j.yexcr.2018.01.012
Publication status	Published - Feb 15 2018

Keywords

Angiotensin II
Calcium channels
E4 promoter-binding protein 4
Hypertrophy

ASJC Scopus subject areas

Cell Biology

Access to Document

10.1016/j.yexcr.2018.01.012

Cite this

Chen, B. C., Shibu, M. A., Kuo, C. H., Shen, C. Y., Chang-Lee, S. N., Lai, C. H., Chen, R. J., Yao, C. H., Viswanadha, V. P., Liu, J. S., Chen, W. K., & Huang, C. Y. (2018). E4BP4 inhibits AngII-induced apoptosis in H9c2 cardiomyoblasts by activating the PI3K-Akt pathway and promoting calcium uptake. Experimental Cell Research, 363(2), 227-234. https://doi.org/10.1016/j.yexcr.2018.01.012

@article{5f2b0319688a4ccc88627fbbd31d5237,

title = "E4BP4 inhibits AngII-induced apoptosis in H9c2 cardiomyoblasts by activating the PI3K-Akt pathway and promoting calcium uptake",

abstract = "The bZIP transcription factor E4BP4 is a survival factor that is known to be elevated in diseased heart and promote cell survival. In this study the role of E4BP4 on angiotensin-II (AngII)-induced apoptosis has been examined in in vitro cell model. H9c2 cardiomyoblast cells that overexpressed E4BP4 were exposed to AngII to observe the cardio-protective effects of E4BP4 on hypertension related apoptosis. The results from TUNEL assays revealed that E4BP4 significantly attenuated AngII-induced apoptosis. Further analysis by Western blot and RT-PCR showed that E4BP4 inhibited AngII-induced IGF-II mRNA expression and cleavage of caspase-3 through the PI3K-Akt pathway. In addition, E4BP4 enhanced calcium reuptake into the sacroplasmic reticulum by down-regulating PP2A and by up-regulating the phosphorylation of PKA and PLB proteins. Our findings indicate that E4BP4 functions as a survival factor in cardiomyoblasts by inhibiting IGF-II transcription and by regulating calcium cycling.",

keywords = "Angiotensin II, Calcium channels, E4 promoter-binding protein 4, Hypertrophy",

author = "Chen, {Bih Cheng} and Shibu, {Marthandam Asokan} and Kuo, {Chia Hua} and Shen, {Chia Yao} and Chang-Lee, {Shu Nu} and Lai, {Chao Hung} and Chen, {Ray Jade} and Yao, {Chun Hsu} and Viswanadha, {Vijaya Padma} and Liu, {Jian Shen} and Chen, {Wei Kung} and Huang, {Chih Yang}",

note = "Funding Information: This study was supported by Taiwan Ministry of Health and Welfare Clinical Trial and Research Center of Excellence ( MOHW106-TDU- B-212-113004 ) Publisher Copyright: {\textcopyright} 2018 Elsevier Inc.",

year = "2018",

month = feb,

day = "15",

doi = "10.1016/j.yexcr.2018.01.012",

language = "English",

volume = "363",

pages = "227--234",

journal = "Experimental Cell Research",

issn = "0014-4827",

publisher = "Elsevier Inc.",

number = "2",

}

TY - JOUR

T1 - E4BP4 inhibits AngII-induced apoptosis in H9c2 cardiomyoblasts by activating the PI3K-Akt pathway and promoting calcium uptake

AU - Chen, Bih Cheng

AU - Shibu, Marthandam Asokan

AU - Kuo, Chia Hua

AU - Shen, Chia Yao

AU - Chang-Lee, Shu Nu

AU - Lai, Chao Hung

AU - Chen, Ray Jade

AU - Yao, Chun Hsu

AU - Viswanadha, Vijaya Padma

AU - Liu, Jian Shen

AU - Chen, Wei Kung

AU - Huang, Chih Yang

N1 - Funding Information: This study was supported by Taiwan Ministry of Health and Welfare Clinical Trial and Research Center of Excellence ( MOHW106-TDU- B-212-113004 ) Publisher Copyright: © 2018 Elsevier Inc.

PY - 2018/2/15

Y1 - 2018/2/15

N2 - The bZIP transcription factor E4BP4 is a survival factor that is known to be elevated in diseased heart and promote cell survival. In this study the role of E4BP4 on angiotensin-II (AngII)-induced apoptosis has been examined in in vitro cell model. H9c2 cardiomyoblast cells that overexpressed E4BP4 were exposed to AngII to observe the cardio-protective effects of E4BP4 on hypertension related apoptosis. The results from TUNEL assays revealed that E4BP4 significantly attenuated AngII-induced apoptosis. Further analysis by Western blot and RT-PCR showed that E4BP4 inhibited AngII-induced IGF-II mRNA expression and cleavage of caspase-3 through the PI3K-Akt pathway. In addition, E4BP4 enhanced calcium reuptake into the sacroplasmic reticulum by down-regulating PP2A and by up-regulating the phosphorylation of PKA and PLB proteins. Our findings indicate that E4BP4 functions as a survival factor in cardiomyoblasts by inhibiting IGF-II transcription and by regulating calcium cycling.

AB - The bZIP transcription factor E4BP4 is a survival factor that is known to be elevated in diseased heart and promote cell survival. In this study the role of E4BP4 on angiotensin-II (AngII)-induced apoptosis has been examined in in vitro cell model. H9c2 cardiomyoblast cells that overexpressed E4BP4 were exposed to AngII to observe the cardio-protective effects of E4BP4 on hypertension related apoptosis. The results from TUNEL assays revealed that E4BP4 significantly attenuated AngII-induced apoptosis. Further analysis by Western blot and RT-PCR showed that E4BP4 inhibited AngII-induced IGF-II mRNA expression and cleavage of caspase-3 through the PI3K-Akt pathway. In addition, E4BP4 enhanced calcium reuptake into the sacroplasmic reticulum by down-regulating PP2A and by up-regulating the phosphorylation of PKA and PLB proteins. Our findings indicate that E4BP4 functions as a survival factor in cardiomyoblasts by inhibiting IGF-II transcription and by regulating calcium cycling.

KW - Angiotensin II

KW - Calcium channels

KW - E4 promoter-binding protein 4

KW - Hypertrophy

UR - http://www.scopus.com/inward/record.url?scp=85040528958&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85040528958&partnerID=8YFLogxK

U2 - 10.1016/j.yexcr.2018.01.012

DO - 10.1016/j.yexcr.2018.01.012

M3 - Article

AN - SCOPUS:85040528958

SN - 0014-4827

VL - 363

SP - 227

EP - 234

JO - Experimental Cell Research

JF - Experimental Cell Research

IS - 2

ER -

E4BP4 inhibits AngII-induced apoptosis in H9c2 cardiomyoblasts by activating the PI3K-Akt pathway and promoting calcium uptake

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this