Histone Deacetylase 2 Is Upregulated in Normal and Keloid Scars

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Histone Deacetylase 2 Is Upregulated in Normal and Keloid Scars Edmund J. Fitzgerald O'Connor, Irbaz I. Badshah, Lucy Y. Addae, Preeya Kundasamy, Sukanthini Thanabalasingam, Daniel Abioye, Mark Soldin, Tanya J. Shaw Journal of Investigative Dermatology Volume 132, Issue 4, Pages 1293-1296 (April 2012) DOI: 10.1038/jid.2011.432 Copyright © 2012 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 1 Immunohistochemistry (IHC) reveals histone deacetylase (HDAC)2 upregulation in human scar tissue. (a) Formalin-fixed, paraffin-embedded human scar samples were analyzed by IHC for expression of HDAC1, 2, 4, and 7. At least three independent reviewers scored the staining intensity and the percentage of positive dermal fibroblast cells in normal skin and scar tissue. The product of these two numbers (mean of 3/4 scorers) gave the IHC score, which was statistically analyzed and is graphically represented. Results were analyzed by paired (normal scars) or unpaired t-tests (keloids); *, P<0.005 (n=10); **, P<0.0001 (n=11). (b, c) Representative patient samples showing HDAC2 upregulation in (b) normal scar tissue, and (c) keloid scars are shown. Brown staining indicates HDAC2 positivity, omission of the primary antibody served as a negative control. Bars=50μm. Journal of Investigative Dermatology 2012 132, 1293-1296DOI: (10.1038/jid.2011.432) Copyright © 2012 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 2 Transforming growth factor (TGF)β1 and cell density may regulate histone deacetylase (HDAC)2 expression in scar tissue. (a) Immunohistochemistry of scars resulting from a 4-mm punch biopsy wound made to the dorsal skin of adult male mice showed elevated HDAC2 expression (brown) in the scar-associated fibroblasts throughout the time course of scar formation. Omission of the primary antibody served as a negative control. Bars=50μm. (b) Western blot analysis of normal human dermal fibroblasts (nHDF, < passage 15) treated with the indicated concentrations of TGFβ1 for 24h, or cultured at varying densities (approximately 25, 50, 75, and 100% confluence) for 96h, revealed a “concentration”-dependent increase in HDAC2 expression. (c) TGFβ1 (1ngml-1) stimulation of Swiss 3T3 (S3T3) cells also resulted in upregulation of HDAC2, as well as an increase in HDAC1 and 7. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) served as a loading control. Journal of Investigative Dermatology 2012 132, 1293-1296DOI: (10.1038/jid.2011.432) Copyright © 2012 The Society for Investigative Dermatology, Inc Terms and Conditions