Molecular and Cellular Biochemistry

, Volume 345, Issue 1, pp 241–247

BNIP3 induces IL6 and calcineurin/NFAT3 hypertrophic-related pathways in H9c2 cardiomyoblast cells

  • Yi-Jiun Weng
  • Wei-Wen Kuo
  • Chia-Hua Kuo
  • Kwong-Chung Tung
  • Chang-Hai Tsai
  • James A. Lin
  • Fuu-Jen Tsai
  • Dennis Jine-Yuan Hsieh
  • Chih-Yang Huang
  • Jin-Ming Hwang
Article

DOI: 10.1007/s11010-010-0578-3

Cite this article as:
Weng, YJ., Kuo, WW., Kuo, CH. et al. Mol Cell Biochem (2010) 345: 241. doi:10.1007/s11010-010-0578-3

Abstract

Ischemia/reperfusion injury causes cardiomyocyte apoptosis, ventricular remodeling, leading to a dilated heart. Hypoxia is one of the causes involved in ischemia damage, and BNIP3 is a hypoxia-inducible marker and also a sensor to induce mitochondria-dependent apoptosis. Recent reports discussed ablating BNIP3 can restrain cardiomyocytes apoptosis and post-infarction remodeling. BNIP3 is a crucial therapeutic target. However, the BNIP3-induced hypertrophy aspect is rarely investigated. Here, we transiently transfected BNIP3 plasmids into H9c2 cardiomyoblast cells to evaluate the molecular signaling and hypertrophy markers using Western blot. We measured the cell size change using actin staining. We disclose that BNIP3 overexpression induced an increase in cell size, activated the pathological-related hypertrophy signaling pathways, such as IL6-MEK5-ERK5, IL6-JAK2-STAT1/3, calcineurin/NFAT3 and p38β MAPK resulting in the fetal genes, ANP and BNP expressing. Concluding above, BNIP3 acts as a pathological hypertrophy inducer, which might be a potential therapeutic target for heart damage prevention.

Keywords

BNIP3 Hypertrophy NFAT3 IL6 H9c2 cardiomyoblast cells 

Abbreviations

ANP

Atrial natriuretic peptide

BNP

B-type natriuretic peptide

ERK5

Extracellular-regulated kinase 5

IL6

Interleukin-6

JAK2

Janus kinase 2

β-MHC

β-Myosin heavy chain

MAPK

Mitogen-activated protein kinase

NFAT3

Nuclear factor of activated T cells 3

STAT1/3

Signal transducers and activators of transcription-1,-3

Copyright information

© Springer Science+Business Media, LLC. 2010

Authors and Affiliations

  • Yi-Jiun Weng
    • 1
  • Wei-Wen Kuo
    • 2
  • Chia-Hua Kuo
    • 3
  • Kwong-Chung Tung
    • 1
  • Chang-Hai Tsai
    • 4
  • James A. Lin
    • 5
  • Fuu-Jen Tsai
    • 6
  • Dennis Jine-Yuan Hsieh
    • 7
  • Chih-Yang Huang
    • 5
    • 6
    • 8
  • Jin-Ming Hwang
    • 9
  1. 1.Department of Veterinary MedicineNational Chung-Hsing UniversityTaichung 402Taiwan, ROC
  2. 2.Department of Biological Science and TechnologyChina Medical UniversityTaichung 404Taiwan, ROC
  3. 3.Laboratory of Exercise BiochemistryTaipei Physical Education CollegeTaipei 105Taiwan, ROC
  4. 4.Department of Healthcare AdministrationAsia UniversityTaichungTaiwan, ROC
  5. 5.Graduate Institute of Basic Medical ScienceTaichungTaiwan, ROC
  6. 6.Department of Chinese MedicineChina Medical UniversityTaichung 404Taiwan, ROC
  7. 7.School of Medical TechnologyChung Shan Medical UniversityTaichung 402Taiwan, ROC
  8. 8.Department of Health and Nutrition BiotechnologyAsia UniversityTaichungTaiwan, ROC
  9. 9.School of Applied ChemistryChung Shan Medical UniversityTaichung 402Taiwan, ROC

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