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. Author manuscript; available in PMC: 2013 Jan 1.

Published in final edited form as: Microvasc Res. 2011 Apr 22;83(1):12–21. doi: 10.1016/j.mvr.2011.04.005

Confluent lung microvascular endothelial cells (LMVEC) were treated with vehicle (DMSO) or 10μM rottlerin for 30 minutes (panel a) or infected with adenoviral vectors encoding GFP or wild-type PKCδ cDNA (panel b). Cells were harvested and p190 activity determined as the level of p190 bound to GST-fused constitutively actvated RhoA. The level of active p190 relative to total p190 was determined by densitometry. In panel b, GFP and PKCδ overexpression was confirmed in the transfected endothelial cells by immunoblot analysis. Data are presented as the mean±SE. Panel a, n=4; ^*p<0.05 vs. vehicle. Panel b, n=7, ^#p<0.05 vs. GFP. Panels a and b: Reprinted from Fordjour, A.K. and Harrington, E.O. 2009. PKCδ influences p190 phosphorylation and activity: Events independent of PKCδ-mediated regulation of endothelial cell stress fiber and focal adhesion formation and barrier function. Biochimica et Biophysica Acta, 1790:1179–1190.

Confluent lung microvascular endothelial cells (LMVEC) were treated with vehicle (DMSO) or 10μM rottlerin for 30 minutes (panel a) or infected with adenoviral vectors encoding GFP or wild-type PKCδ cDNA (panel b). Cells were harvested and p190 activity determined as the level of p190 bound to GST-fused constitutively actvated RhoA. The level of active p190 relative to total p190 was determined by densitometry. In panel b, GFP and PKCδ overexpression was confirmed in the transfected endothelial cells by immunoblot analysis. Data are presented as the mean±SE. Panel a, n=4; ^*p<0.05 vs. vehicle. Panel b, n=7, ^#p<0.05 vs. GFP. Panels a and b: Reprinted from Fordjour, A.K. and Harrington, E.O. 2009. PKCδ influences p190 phosphorylation and activity: Events independent of PKCδ-mediated regulation of endothelial cell stress fiber and focal adhesion formation and barrier function. Biochimica et Biophysica Acta, 1790:1179–1190.