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. Author manuscript; available in PMC: 2011 Jun 1.
Published in final edited form as: Int J Biochem Cell Biol. 2010 Feb 23;42(6):965–974. doi: 10.1016/j.biocel.2010.02.009

Figure 5. Hyperglycemia-induced activation of Rap1 promotes the association of Itgβ3 and PKCβ.

Figure 5

SMCs cultured under hyperglycemic conditions have elevated active Rap1 as measured by pull-down assay described in the Methods section (A). The activation of Rap1 by hyperglycemia could be attenuated by targeting Rap1 expression with siRNA to Rap1a and Rap1b or to the Rap1 CalDAG-GEF (A). Loss of Rap1 activation reduces the association of PKCβ with integrin β3 immunoprecipitates (B). The association of PKCβ with integrin β3 is not observed in aortas from diabetic Rap1a−/− and Rap1b−/− mice (C). Downregulation of Rap1 signaling attenuates ERK activation in SMC cultured in hyperglycemic conditions (D). (E) TSP-1 induced ERK activation was abolished in Rap1b−/− SMC cells. Results are representative of those obtained in 3 – 5 independent experiments.