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. 2012 Dec 21;14(1):255–272. doi: 10.3390/ijms14010255

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© 2013 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).

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CrAT gene silencing attenuates shear stress induced NO signaling in pulmonary arterial endothelial cells. PAEC were transiently transfected with a scrambled siRNA or a specific CrAT siRNA for 48 h then acutely exposed to laminar shear stress (20 dyn/cm², 15 min) in the presence or absence of the NOS inhibitor 2-ethyl-2-thiopseudourea (ETU; 100 μM, 30 min) and the effect on eNOS-derived superoxide generation determined by EPR (A) Decreasing CrAT activity significantly increased superoxide levels. The presence of ETU significantly inhibited the increase in superoxide levels in the CrAT siRNA transfected cells, indicating that it is eNOS-dependent (B) Conversely, the shear-mediated increase in NO_x was significantly decreased in CrAT siRNA transfected PAEC. Values are mean ± SEM; N = 6; * p < 0.05 vs. scrambled siRNA.