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Current Molecular Medicine

Editor-in-Chief

ISSN (Print): 1566-5240
ISSN (Online): 1875-5666

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

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

Volume 16 , Issue 5 , 2016

Page: [515 - 523] Pages: 9

DOI: 10.2174/1566524016666160523143704

Price: $65

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).


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