Key result
Pharmacologic inhibition of EGFR prevented the cytokine-induced increase in urea production and arginase expression in bovine pulmonary arterial endothelial cells without affecting nitric oxide production.
p-value: p=<0.05
EGFR inhibitors attenuate cytokine-induced arginase expression in pulmonary endothelial cells without affecting NO release, suggesting a potential therapeutic target for vascular remodeling in pulmonary hypertension.
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Should not yet change pulmonary hypertension practice; hypothesis-generating for EGFR as a selective target in endothelial remodeling.
Nelin et al. (2005) studied Pulmonary hypertension (in vitro model). EGFR inhibitors (genistein or AG1478) during cytokine (LPS/TNF-alpha) stimulation vs. Cytokine stimulation alone and vehicle control was evaluated on Urea production and arginase I/II expression (p=<0.05). Pharmacologic inhibition of EGFR prevented the cytokine-induced increase in urea production and arginase expression in bovine pulmonary arterial endothelial cells without affecting nitric oxide production.
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