Cardiac Specific Overexpression of hHole Attenuates Isoproterenol–Induced Hypertrophic Remodeling through Inhibition of Extracellular Signal-Regulated Kinases (ERKs) Signalling

Author(s): W. Xu, Y. Wang, J. Zhou, X. Zhu, S. Zhang, W. Yuan, X. Liu, Y. Shi, L. Cao, Q. Zeng, Z. Jiang, X. Ye, Y. Wan, X. Peng, Y. Deng, F. Chen, X. Wang, G. Dai, S. Luo, X. Fan, X. Mo, X. Wu, Y. Li

Journal Name: Current Molecular Medicine

Volume 16 , Issue 5 , 2016

  Journal Home
Translate in Chinese
Become EABM
Become Reviewer

Abstract:

The human Hole gene (hHole) encodes a six-transmembrane protein with 319- amino acids. Our previous study showed that hHole was strongly expressed in adult heart and may act as a suppressor of extracellular signal-regulated kinases (ERKs), overactivation of which contributed to pathological cardiac hypertrophy. In this study, it was observed that Hole expression was up-regulated in murine hypertrophic hearts. In a cardiac specific transgenic mouse model, it was observed that overexpression of hHole specifically in heart attenuated cardiac hypertrophy and fibrosis induced by isoproterenol (ISO), with blunted transcriptions of ERK1/2, total ERK1/2 proteins and phosphorylated ERK1/2 (p-ERK1/2) levels. Furthermore, overexpression of hHole in mice by hydrodynamic tail-vein injection with hHole plamids also inhibited cardiac hypertrophy induced by ISO. Our work identified hHole as a novel repressor of cardiac hypertrophy, and provided new insights into the possible target for the prevention or treatment of cardiac diseases.

Keywords: Cardiac hypertrophy, human Hole gene (hHole), isoproterenol (ISO), extracellular signal-regulated kinases (ERKs).

Rights & PermissionsPrintExport Cite as

Article Details

VOLUME: 16
ISSUE: 5
Year: 2016
Page: [515 - 523]
Pages: 9
DOI: 10.2174/1566524016666160523143704
Price: $65

Article Metrics

PDF: 27
HTML: 3