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

Autor: Chen BC; School of Post-Baccalaureate Chinese Medicine, China Medical University, Taichung, Taiwan., Shibu MA; Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan., Kuo CH; Laboratory of Exercise Biochemistry, University of Taipei, Taipei, Taiwan., Shen CY; Department of Nursing, Meiho University, Pingtung, Taiwan., Chang-Lee SN; Department of Healthcare Administration, Asia University, Taiwan., Lai CH; Division of Cardiology, Department of Internal Medicine, Armed Force Taichung, General Hospital, Taichung 41152, Taiwan., Chen RJ; Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan., Yao CH; Department of Biomedical Imaging and Radiological Science, China Medical University, Taichung, Taiwan., Viswanadha VP; Department of Biotechnology, Bharathiar University, Coimbatore 641046, India., Liu JS; Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, China Medical University Beigang Hospital, Yunlin County, Taiwan; Department of Emergency Medicine, China Medical University Hospital, Taichung, Taiwan., Chen WK; School of Post-Baccalaureate Chinese Medicine, China Medical University, Taichung, Taiwan., Huang CY; Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan; Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan; Graduate Institute of Chinese Medical Science, China Medical University, Taichung, Taiwan. Electronic address: cyhuang@mail.cmu.edu.tw.
Jazyk: angličtina
Zdroj: Experimental cell research [Exp Cell Res] 2018 Feb 15; Vol. 363 (2), pp. 227-234. Date of Electronic Publication: 2018 Jan 10.
DOI: 10.1016/j.yexcr.2018.01.012
Abstrakt: 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.)
Databáze: MEDLINE
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