Open Access

The role of mAKAPβ in the process of cardiomyocyte hypertrophy induced by angiotensin II

  • Authors:
    • Huixin Guo
    • Baoxin Liu
    • Lei Hou
    • Erlinda The
    • Gang Li
    • Dongzhi Wang
    • Qiqiang Jie
    • Wenliang Che
    • Yidong Wei
  • View Affiliations

  • Published online on: March 2, 2015     https://doi.org/10.3892/ijmm.2015.2119
  • Pages: 1159-1168
  • Copyright: © Guo et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

Angiotensin II (AngII) is the central product of the renin‑angiotensin system (RAS) and this octapeptide contributes to the pathophysiology of cardiac hypertrophy and remodeling. mAKAPβ is an A‑kinase anchoring protein (AKAP) that has the function of binding to the regulatory subunit of protein kinase A (PKA) and confining the holoenzyme to discrete locations within the cell. In this study, we aimed to investigate the role of mAKAPβ in AngII‑induced cardiomyocyte hypertrophy and the possible mechanisms involved. Cultured cardiomyocytes from neonatal rats were treated with AngII. Subsequently, the morphology of the cardiomyocytes was observed and the expression of mAKAPβ and cardiomyocyte hypertrophic markers was measured. mAKAPβ‑shRNA was constructed for RNA interference; the expression of mAKAPβ and hypertrophic markers, the cell surface area and the [3H]Leucine incorporation rate in the AngII‑treated rat cardiomyocytes were detected following RNA interference. Simultaneously, changes in the expression levels of phosphorylated extracellular signal-regulated kinase (p‑ERK)2 in the cardiomyocytes were assessed. The cell size of the AngII-treated cardiaomyocytes was significantly larger than that of the untreated cardiomyocytes. The expression of hypertrophic markers and p‑ERK2, the cell surface area and the [3H]Leucine incorporation rate were all significantly increased in the AngII‑treated cells. However, the expression of mAKAPβ remained unaltered in this process. RNA interference simultaneously inhibited the protein expression of mAKAPβ and p‑ERK2, and the hypertrophy of the cardiomyocytes induced by AngII was attenuated. These results demonstrate that AngII induces hypertrophy in cardiomyocytes, and mAKAPβ is possibly involved in this process. The effects of mAKAPβ on AngII‑induced cardiomyocyte hypertrophy may be associated with p‑ERK2 expression.
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May-2015
Volume 35 Issue 5

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Guo H, Liu B, Hou L, The E, Li G, Wang D, Jie Q, Che W and Wei Y: The role of mAKAPβ in the process of cardiomyocyte hypertrophy induced by angiotensin II. Int J Mol Med 35: 1159-1168, 2015
APA
Guo, H., Liu, B., Hou, L., The, E., Li, G., Wang, D. ... Wei, Y. (2015). The role of mAKAPβ in the process of cardiomyocyte hypertrophy induced by angiotensin II. International Journal of Molecular Medicine, 35, 1159-1168. https://doi.org/10.3892/ijmm.2015.2119
MLA
Guo, H., Liu, B., Hou, L., The, E., Li, G., Wang, D., Jie, Q., Che, W., Wei, Y."The role of mAKAPβ in the process of cardiomyocyte hypertrophy induced by angiotensin II". International Journal of Molecular Medicine 35.5 (2015): 1159-1168.
Chicago
Guo, H., Liu, B., Hou, L., The, E., Li, G., Wang, D., Jie, Q., Che, W., Wei, Y."The role of mAKAPβ in the process of cardiomyocyte hypertrophy induced by angiotensin II". International Journal of Molecular Medicine 35, no. 5 (2015): 1159-1168. https://doi.org/10.3892/ijmm.2015.2119