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 journalArticle

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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 languageEnglish
JournalExperimental Cell Research
DOIs
Publication statusAccepted/In press - Jan 1 2018

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Phosphatidylinositol 3-Kinases
Angiotensin II
Apoptosis
Calcium
Insulin-Like Growth Factor II
Basic-Leucine Zipper Transcription Factors
Far-Western Blotting
Reticulum
In Situ Nick-End Labeling
Caspase 3
Heart Diseases
Cell Survival
Phosphorylation
Hypertension
Polymerase Chain Reaction
Messenger RNA
Proteins

Keywords

  • Angiotensin II
  • Calcium channels
  • E4 promoter-binding protein 4
  • Hypertrophy

ASJC Scopus subject areas

  • Cell Biology

Cite this

E4BP4 inhibits AngII-induced apoptosis in H9c2 cardiomyoblasts by activating the PI3K-Akt pathway and promoting calcium uptake. / Chen, Bih Cheng; Shibu, Marthandam Asokan; Kuo, Chia Hua; Shen, Chia Yao; Chang-Lee, Shu Nu; Lai, Chao Hung; Chen, Ray Jade; Yao, Chun Hsu; Viswanadha, Vijaya Padma; Liu, Jian Shen; Chen, Wei Kung; Huang, Chih Yang.

In: Experimental Cell Research, 01.01.2018.

Research output: Contribution to journalArticle

Chen, Bih Cheng ; Shibu, Marthandam Asokan ; Kuo, Chia Hua ; Shen, Chia Yao ; Chang-Lee, Shu Nu ; Lai, Chao Hung ; Chen, Ray Jade ; Yao, Chun Hsu ; Viswanadha, Vijaya Padma ; Liu, Jian Shen ; Chen, Wei Kung ; Huang, Chih Yang. / E4BP4 inhibits AngII-induced apoptosis in H9c2 cardiomyoblasts by activating the PI3K-Akt pathway and promoting calcium uptake. In: Experimental Cell Research. 2018.
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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.",
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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

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