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

[ Vol. 16 , Issue. 5 ]


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 and Y. Li   Pages 515 - 523 ( 9 )


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.


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


The Center for Heart Development, Key Lab of MOE for Development Biology and Protein Chemistry, College of Life Sciences, Hunan Normal University, Changsha 410081, China.

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