Key result
Endothelin-1 induces a glycolytic switch in pulmonary arterial endothelial cells via the redistribution of uncoupled eNOS to the mitochondria, mediated by PKC delta-dependent phosphorylation.
Why the study?
Does Endothelin-1 induce a glycolytic switch in pulmonary arterial endothelial cells via eNOS mitochondrial translocation?
Population
Ovine pulmonary arterial endothelial cells (PAECs) and monocrotaline (MCT) rat model of pulmonary hypertension
Comparison
Endothelin-1 exposure in vitro; Monocrotaline… vs Untreated PAECs; control rats
Design
Preclinical
Follow-up
Up to 28 days post-MCT in rats; 4 hours for ET-1 in cells
Authors
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ET-1-driven endothelial glycolysis untested in humans; leaves open PKCδ as a PH target.
Does Endothelin-1 induce a glycolytic switch in pulmonary arterial endothelial cells via eNOS mitochondrial translocation?
p-value: p=<0.05
ET-1 induces a glycolytic switch in pulmonary arterial endothelial cells via eNOS mitochondrial translocation, identifying a potential mechanistic target for treating pulmonary hypertension.
Sun et al. (2014) studied Pulmonary Hypertension. Endothelin-1 vs. Untreated/Control was evaluated on Mitochondrial bioenergetics and eNOS translocation (p=<0.05). Endothelin-1 induces a glycolytic switch in pulmonary arterial endothelial cells via the redistribution of uncoupled eNOS to the mitochondria, mediated by PKC delta-dependent phosphorylation.
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