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. 2013 May 31;305(3):L240–L255. doi: 10.1152/ajplung.00355.2012

Fig. 6.

Fig. 6.

Depletion of PKC isoforms inhibits thrombin-induced ERM and MLC phosphorylation. Confluent HPAEC were incubated with nonspecific and PKCβI-, PKCζ-, PKCθ-, PKCδ-, PKCγ-, and PKCε-specific siRNA (A) or with nonspecific, combinations of PKCδ- and PKCε-specific, combinations of PKCγ-, PKCδ-, and PKCε-specific, and combinations of PKCβI-, PKCθ-, and PKCζ-specific siRNAs (C) as described in materials and methods and then stimulated by thrombin (0.5 U/ml, 5 min) or vehicle. Total lysates were analyzed by immunoblotting for phospho-ERM or di-phospho-MLC (Thr18/Ser19). Immunoblotting with β-tubulin Ab was used as a normalization control. Rearranged lanes from the same blot are outlined by vertical dotted line. B, D, and E: bar graphs represent relative densitometry of fold changes in phosphorylated ERM and MLC after thrombin relative to vehicle-treated control. Results are means ± SE of 4 independent experiments. *Significantly different from cells treated with ns siRNA without thrombin (P < 0.01); #significantly different from cells treated with ns siRNA without thrombin (P < 0.05). **Significantly different from cells treated with ns siRNA and thrombin (P < 0.05).