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. 2004 May 24;142(4):737–748. doi: 10.1038/sj.bjp.0705829

Figure 2.

Figure 2

Activation of PKC is involved in PGF2α and Butaprost-induced upregulation of Nur77 mRNA expression. hFP-HEK 293/EBNA cells or hEP2-HEK 293/EBNA cells were pretreated with a Rho inhibitor (Clostridium difficile Toxin B, 100 ng ml−1), a PKC inhibitor (GF109203 X, 2.5 μM), an MAPK inhibitor (PD 98059, 20 μM), or a Ca2+ chelator (BAPTA, 2.5 μM) for 30 min, followed by continued incubation with 10−7 M PGF2α (a) or Butaprost (b) for 6 h. Arrows indicate Nur77 mRNA levels and 28s and 18s rRNA (a and b, top panels). The intensity of 28s and 18s rRNA bands was used as an internal control to normalize RNA loading differences. The data represent mean±s.d. of three independent experiments (a and b, bottom panels). *P<0.01 vs control; **P<0.05 vs PGF2α alone; ***P<0.01 vs PGF2α or Butaprost alone.