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. 2013 Mar 5;288(16):11004–11012. doi: 10.1074/jbc.M112.441816

FIGURE 5.

FIGURE 5.

In vivo HDAC2 knockdown by siRNAs and the inhibition of NO synthesis by L-NAME show opposite effects on skin repair. A, graph showing kinetics of skin wound healing in CD1 mice treated topically with siRNA specific for HDAC2 alone (n = 8) or in combination with Sirtinol (n = 7) or MC2652 (n = 7). Scrambled RNA oligos (n = 8) and TSA (n = 7) were used as controls. B, immunofluorescence showing HDAC2 expression (red). Nuclei were counterstained with Hoechst (blue) (magnification ×20). $ and ^, p < 0.05 versus scrambled. C, L-NAME prevents SIRT-dependent skin regeneration in the kinetics of wound healing. CD1 mice were treated with Resv (n = 13), MC2562 (n = 12), L-NAME (n = 8), and L-NAME in combination with Resv (n = 8) or MC2562 (n = 7). DMSO was used as a control solvent (n = 10). *, °, and &, p < 0.05 versus solvent. D, immunoprecipitation analysis of HDAC2 cysteine nitrosylation (SNO-Cys) in presence of the general inhibitor of NO synthesis l-NAME alone or in combination with SIRT activators. Relative densitometries respect input are shown in right. *, °, and &, p < 0.05 versus solvent.