Key result
Endothelin-1 treatment of fetal cardiomyocytes significantly altered 75 proteins, highlighting key proliferation regulators including EED, UBC, ERK1/2, MAPK, Akt, and EGFR.
ET-1 induces significant proteomic changes in fetal cardiomyocytes, suggesting a mechanism for premature terminal differentiation involving epigenetic regulators like EED.
May caution against ET-1 elevation in fetal hypoxia; leaves open specific proteomic drivers of cardiomyocyte differentiation.
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.
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Shin et al. (2017) studied Fetal cardiomyocyte terminal differentiation. Endothelin-1 (ET-1) was evaluated on Proteomic alterations. Endothelin-1 treatment of fetal cardiomyocytes significantly altered 75 proteins, highlighting key proliferation regulators including EED, UBC, ERK1/2, MAPK, Akt, and EGFR.
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