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. Author manuscript; available in PMC: 2016 Oct 1.
Published in final edited form as: Exp Dermatol. 2015 Aug 18;24(10):773–778. doi: 10.1111/exd.12762

Fig 3. Deficiency of SIRT6 aggravates oxidative stress and markedly impairs wound vascularity in diabetic mice.

Fig 3

(A–C) Representative western immunoblots and densitometry analysis using Image Quant software for p47 phox and p67 phox in SIRT6-KD and control diabetic wounds; Blots were normalized against Actin. White and black bars represent Control and SIRT6-KD diabetic wounds respectively. (D–E) Immunohistochemical staining for CD31 demonstrate reduced expression of CD31 within SIRT6-KD wound beds compared with nonsense-treated wounds at postwounding day 14. (F) Bar graph showing the number of CD31 positive cells (20 fields) in SIRT6-KD and control diabetic wounds. (G–H) Immunohistochemical staining of VEGF shows reduced expression of VEGF positive cells in the SIRT6-KD treated diabetic wounds compared to non sense treated. (I) Bar graph showing number of VEGF positive cells in SIRT6-KD and control diabetic wounds. Representative results from three independent experiments with three-four animals in each group are shown. Values are means ± SEM. *p < 0.05 ; **p < 0.01 vs. Control diabetic wounds on the same day.