hHole基因在心脏特异性过度表达抑制由异丙肾上腺素诱导的心肌肥厚重构–通过抑制细胞外信号调节激酶（ERK）的信令

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

Volume: 16 Issue: 5

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 and F. Chen, X. Wang, G. Dai, S. Luo, X. Fan, X. Mo, X. Wu, Y. Li

Affiliation:

关键词: 心肌肥厚；人Hole基因（hHole）；异丙肾上腺素（ISO）；细胞外信号调节激酶（ERK）。

摘要: 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.

Cite this article as:

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 and F. Chen, X. Wang, G. Dai, S. Luo, X. Fan, X. Mo, X. Wu, Y. Li , Cardiac Specific Overexpression of hHole Attenuates Isoproterenol–Induced Hypertrophic Remodeling through Inhibition of Extracellular Signal-Regulated Kinases (ERKs) Signalling, Current Molecular Medicine 2016; 16 (5) . https://dx.doi.org/10.2174/1566524016666160523143704