Proteomic Analysis of Endothelin-1 Targets in the Regulation of Cardiomyocyte Proliferation

Author(s): Alexandra N. Shin, Chiranjib Dasgupta, Guangyu Zhang, Kala Seal, Lubo Zhang*

Journal Name: Current Topics in Medicinal Chemistry

Volume 17 , Issue 15 , 2017

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Graphical Abstract:


Hypoxia is a fetal stressor that leads to the production of endothelin-1 (ET-1). Previous work has shown that ET-1 treatment leads to the premature terminal differentiation of fetal cardiomyocytes. However, the precise mechanism is unknown. We tested the hypothesis that the fetal cardiomyocyte proteome will be greatly altered due to ET-1-treatment, which reveals a potential molecular mechanism of ET-1-induced terminal differentiation. Over a thousand proteins were detected in the fetal cardiomyocytes and among them 75 proteins were significantly altered due to ET-1 treatment. Using IPA pathway analysis, the merged network depicted several key proteins that appeared to be involved in regulating proliferation, including: EED, UBC, ERK1/2, MAPK, Akt, and EGFR. EED protein, which is associated with regulating proliferation via epigenetic mechanisms, is of particular interest. Herein we propose a model of the molecular mechanism by which ET-1 induced cardiomyocyte terminal differentiation occurs.

Keywords: Cardiomyocyte, Endothelin-1, EED, Fetal, Heart, Proliferation, Proteome.

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Article Details

Year: 2017
Published on: 26 April, 2017
Page: [1788 - 1802]
Pages: 15
DOI: 10.2174/1568026617666161116142417
Price: $65

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