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. Author manuscript; available in PMC: 2015 Apr 28.
Published in final edited form as: Naunyn Schmiedebergs Arch Pharmacol. 2012 Mar 14;385(5):443–453. doi: 10.1007/s00210-011-0705-z

Fig. 8.

Fig. 8

Increased ERK activity controls proliferation of RGS-insensitive Gαi2 cardiac fibroblasts. Cardiac fibroblasts from wild-type (WT) or Gαi2G184S/G184S mice were grown for 24 h in complete medium without (PTX-) or with (PTX+) PTX. a Representative blot for phospho-ERK and total ERK assessed as in “Methods.” b Densitometric analysis of phospho-ERK/total ERK normalized to the value of the PTX-WT cells. c After growing for 24 h in complete medium, cardiac fibroblasts were starved with serum-free medium overnight, and samples were analyzed for phospho-ERK and total ERK expression. d The effect of the MEK inhibitor PD 98059 on fibroblast number was assessed after 3 days in culture with DMSO or 30 µM PD 98059. Values are mean±SEM for fibroblasts from three different animals with each assay done in duplicate. p<0.05 Gαi2G184S/G184S vs WT cells. *p<0.05 vehicle- vs PTX- or PD 98059-treated cells