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. 2019 Oct 14;8(10):1253. doi: 10.3390/cells8101253

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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(a) HUVECs were stimulated for the indicated times with the MEK inhibitors, AZD6244 or PD032590, in the presence or absence of 100 μM I942. Cell extracts were then prepared and immunoblotted with anti-ERK and phospho-ERK antibodies or anti-ICAM1 antibodies, as indicated. (b) HUVECs were stimulated for the indicated times with the PI3 kinase inhibitor, GDC0941 (10 μM), or the AKT inhibitor, MK2206 (10 μM). Cell extracts were then immunoblotted with anti-AKT and phospho-AKT antibodies or anti-ICAM1 antibody. (c) ICAM1 densitometric values from 3 separate immunoblots are shown as a bar graph with significant changes in ICAM1 expression, relative to cells stimulated with diluent alone being indicated; * p < 0.05, ** p < 0.01, *** p < 0.001.

(a) HUVECs were stimulated for the indicated times with the MEK inhibitors, AZD6244 or PD032590, in the presence or absence of 100 μM I942. Cell extracts were then prepared and immunoblotted with anti-ERK and phospho-ERK antibodies or anti-ICAM1 antibodies, as indicated. (b) HUVECs were stimulated for the indicated times with the PI3 kinase inhibitor, GDC0941 (10 μM), or the AKT inhibitor, MK2206 (10 μM). Cell extracts were then immunoblotted with anti-AKT and phospho-AKT antibodies or anti-ICAM1 antibody. (c) ICAM1 densitometric values from 3 separate immunoblots are shown as a bar graph with significant changes in ICAM1 expression, relative to cells stimulated with diluent alone being indicated; * p < 0.05, ** p < 0.01, *** p < 0.001.