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Fig. 5 | Journal of Translational Medicine

Fig. 5

From: The epigenome as a putative target for skin repair: the HDAC inhibitor Trichostatin A modulates myeloid progenitor plasticity and behavior and improves wound healing

Fig. 5

iHDAC modulates bone marrow myeloid progenitors behavior in vivo and improves wound healing. Inhibition of HDAC activity improves wound healing after 5 days of skin lesion (AE, K). n = 12 animals per group. Data representative of 3 independent experiments. Data are mean ± SD. Statistically significant differences, **p < 0.01, by the two-way ANOVA test followed by the test of Bonferroni to correct the value of p. Both control and iHDAC wounds were positive for Arginase-1 (F, F’), iNOS (G, G’) and H4K16ac (H, H’). Confocal microscopy analysis revealed the presence of very elongated F4/80/H4ac positive cells only when wounds were topically treated with iHDAC (J, inset). Confocal analysis of optical cross sections (j2) in addition to XZ (j3) and YZ (j4) projections highlights that F4/80 + cells (green, j2) and also positive for H4Ac (red, j2). In contrast, confocal analysis of optical cross sections (i2) in addition to XZ (i3) and YZ (i4) projections highlights that macrophages in the control skin were positive only for F4/80. K Wound healing dynamics during 7 days upon skin injury in control and iHDAC treated wounds. L Immunohistochemistry of control and iHDAC treated wounds showing an enrichment of Arginase-1 + cells in control wounds in the dermal layer if compared to iHDAC treated wounds (white arrows, discontinuous epidermal/dermal layer boundary). Western blot quantification analysis showed that iHDAC treated wounds (triplicates T1, T2, T3) presented significant lower levels of Arginase-1 when compared to control group (triplicates C1, C2, C3). N = 4; **p < 0.01, by Test T

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