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

Department of Health and Physical Education (HPE)

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

9 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. Copyright © 2018 Elsevier Inc. All rights reserved.

Original language	English
Pages (from-to)	227-234
Journal	Experimental Cell Research
Volume	363
Issue number	2
Early online date	Jan 2018
DOIs	https://doi.org/10.1016/j.yexcr.2018.01.012
Publication status	Published - 2018

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10.1016/j.yexcr.2018.01.012

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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

CHEN, B-C, SHIBU, MA, KUO, CH, SHEN, C-Y, CHANG-LEE, SN, LAI, C-H, CHEN, R-J, YAO, C-H, VISWANADHA, VP, 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, vol. 363, no. 2, pp. 227-234. https://doi.org/10.1016/j.yexcr.2018.01.012

@article{58e9859000214ada95a3781c38561518,

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. Copyright {\textcopyright} 2018 Elsevier Inc. All rights reserved.",

author = "Bih-Cheng CHEN and SHIBU, \{Marthandam Asokan\} and KUO, \{Chia Hua\} and Chia-Yao SHEN and CHANG-LEE, \{Shu Nu\} and Chao-Hung LAI and Ray-Jade CHEN and Chun-Hsu YAO and VISWANADHA, \{Vijaya Padma\} and Jian-Shen LIU and Wei-Kung CHEN and Chih-Yang HUANG",

year = "2018",

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

language = "English",

volume = "363",

pages = "227--234",

journal = "Experimental Cell Research",

issn = "0014-4827",

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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

PY - 2018

Y1 - 2018

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. Copyright © 2018 Elsevier Inc. All rights reserved.

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. Copyright © 2018 Elsevier Inc. All rights reserved.

UR - https://www.scopus.com/pages/publications/85040528958

U2 - 10.1016/j.yexcr.2018.01.012

DO - 10.1016/j.yexcr.2018.01.012

M3 - Articles

C2 - 29331388

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

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