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. 2011 Apr 5;43(12):749–757. doi: 10.1152/physiolgenomics.00229.2010

Fig. 2.

Fig. 2.

AA induction of Osx expression is independent of p38, MEK, JNK, IGF-I, BMP, and integrin pathways. A–C: effect of IGF-I binding protein-4 (BP-4), noggin, and cyclic Arg-Gly-Asp (RGD) peptide on AA-induced Osx mRNA expression, respectively. Primary osteoblasts or MC3T3-E1 cells were treated with vehicle, BP-4 (300 ng/ml), noggin (250 ng/ml), and RGD (5 μM), respectively, for 24 h prior to RNA extraction and real-time RT-PCR. The results are expressed as fold changes compared with the expression level of vehicle control without AA treatment (n = 3). *P < 0.01 compared with expression levels of corresponding controls in the absence of AA. D: effects of inhibitors of p38, MEK, and JNK signaling pathways on AA-induced osterix expression. MC3T3-E1 cells were treated with DMSO or inhibitors of p38 (200 nM SB-203580), MEK (10 μM U-0126), and JNK (200 nM SP-600125) for 30 min prior to treatment with or without AA. RNA was extracted 24 h later for real time RT-PCR. The results are expressed as fold change compared with the expression level of DMSO control without AA treatment (n = 3). *Statistical significance compared with expression level of corresponding controls in the absence of AA (P < 0.01). **Statistical significance compared with corresponding cells treated with DMSO in the absence of AA (P < 0.05).