Figure 3. Expression of proinflammatory genes in TPA-treated mice. (A) RQ-PCR was performed with cDNA from total wt and Rage−/− skin samples treated once with acetone (0 h) or with 10 nmol TPA in acetone and collected at the indicated time points and by using primers for Mip-1α, Mip-1β, Mip-2, Ptgs2, S100a8, S100a9, Tnf-α, and Tgf-β3. Each cDNA from three mice of three separate animal experiments was analyzed in triplicates, and Hprt transcripts served as an internal reference. Error bars represent the SEM. (B) Representative pictures of sections derived from tissue specimens as described in A and analyzed for S100a9 and Mip-1α protein expression by IHC staining (brown signal) and followed by counterstaining with hematoxylin. Dashed lines indicate the border between the epidermis and dermis. co, acetone-treated controls. Bar, 20 μm.
Figure 3.

Expression of proinflammatory genes in TPA-treated mice. (A) RQ-PCR was performed with cDNA from total wt and Rage−/− skin samples treated once with acetone (0 h) or with 10 nmol TPA in acetone and collected at the indicated time points and by using primers for Mip-1α, Mip-1β, Mip-2, Ptgs2, S100a8, S100a9, Tnf-α, and Tgf-β3. Each cDNA from three mice of three separate animal experiments was analyzed in triplicates, and Hprt transcripts served as an internal reference. Error bars represent the SEM. (B) Representative pictures of sections derived from tissue specimens as described in A and analyzed for S100a9 and Mip-1α protein expression by IHC staining (brown signal) and followed by counterstaining with hematoxylin. Dashed lines indicate the border between the epidermis and dermis. co, acetone-treated controls. Bar, 20 μm.

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