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. Author manuscript; available in PMC: 2016 Aug 1.
Published in final edited form as: J Pathol. 2015 May 12;236(4):433–444. doi: 10.1002/path.4548

Figure 1. Impaired PPAR-γ activity in diabetic wound macrophages.

Figure 1

(A–D) Macrophages (Mp) were isolated from chronic wound biopsies and expression of PPAR-γ, PGC-1β and downstream targets CD36 and CPT-1 assessed by real time PCR. For comparison, blood-derived Mp from healthy volunteers were either left non-stimulated (Non) or stimulated with IL-1β. (EH) Expression of PPAR-γ, PGC-1β and downstream targets in Mp isolated from wounds of non-diabetic (ND) and diabetic (DB) mice on days 5, 10 and 20 post-injury. (I–L) Expression of PPAR-γ, PGC-1β and downstream targets in bone marrow-derived Mp from wild-type mice stimulated with day 5 or 10 wound conditioned medium (CM) from ND or DB mice. (M) Representative flow cytogram of MitoTracker green labeling in Mp (F4/80+ cells) isolated from day 10 ND and DB wounds. (N) Summary data for median fluorescence intensity (MFI) for MitoTracker green in Mp isolated from day 5 and 10 wounds of ND and DB mice. (O) Representative flow cytogram of MitoTracker green labeling in cultured Mp treated with CM from day 10 wounds of ND or DB mice. (P) Summary data for MFI for MitoTracker green in cultured Mp treated with recombinant IL-1β or with CM from day 10 wounds of ND or DB mice. For all graphs, bars = mean + SD, n = 6 for human data and n = 6–8 for mouse data. *mean value significantly different from that for Non controls or 5d values, **mean value for DB significantly different from that for ND at same time point, p < 0.05.