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. Author manuscript; available in PMC: 2018 Mar 28.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2014 Nov 13;35(1):163–174. doi: 10.1161/ATVBAHA.114.304705

Figure 1.

Figure 1

Protein tyrosine phosphatase 1B (PTP1B)−/− mice showed an accelerated diabetic wound healing rate. A, Plasma glucose level in wild-type (WT) and PTP1B−/− mice treated with or without streptozotocin (STZ). B, Body weight of WT and PTP1B−/− mice treated with or without STZ. C, Left, Images of the skin wound in WT, STZ-treated, and STZ-treated PTP1B−/− mice from 0, 7, and 14 days post wounding. Right, Quantitative analysis of wound healing in WT and PTP1B−/− mice treated with or without STZ. The percentage of the wound area at different time point post injury vs the initial wound area was used as an indicator for wound healing measurement. D, Left, Masson trichrome staining and CD31 labeling assay of skin tissues of WT and PTP1B−/− mice treated with or without STZ on day 7 post wounding. Right, Quantitative analysis of the number of CD31+ cells. E, Western blot results showing the PTP1B protein levels of skin tissues in WT and PTP1B−/− mice treated with or without STZ. Images of the Western blot assay were analyzed using the Bandscan software. Data are presented as the mean±SD of ≥3 independent experiments. There were 6 mice in each group per condition. *P<0.05 and **P<0.01.