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. Author manuscript; available in PMC: 2009 Feb 12.

Published in final edited form as: Circ Res. 2008 Jun 19;103(2):e15–e26. doi: 10.1161/CIRCRESAHA.108.177386

Fig. 6 — Unilateral limb ischemia was induced in diabetic and normoglycemic mice before an adenovirus carrying a dominant negative mutant of p75^NTR (Ad.DN-p75^NTR) or Ad.GFP was delivered to the ischemic adductor. (a) Time-course of post-ischemic BF recovery (calculated by laser colour doppler) in diabetics and normoglycemic mice treated with Ad.DN-p75^NTR or Ad.GFP; (b) Representative laser Doppler images taken at 14d after induction of ischemia are shown. Squares include the area of interest; (c) Recovery of BF (measured by Oxford Optronic) to the ischemic adductor (expressed as the ration between BF in the ischemic to BF in the contra-lateral muscle) at 14d after ischemia induction. Values are mean±SEM. *P<0.05 vs. healthy with Ad.GFP, ^§P<0.05 versus diabetic with Ad.GFP. (d) Capillary density in the ischemic adductor at 14d post-ischemia. Values are means±SEM. **P<0.01 vs. healthy with Ad.GFP, ^§§P<0.05 vs. diabetic with Ad.GFP. (e) Apoptosis (revealed by TUNEL assay) and (f) proliferation (revealed by immunhistochemistry for the proliferation antigen MCM-2) of capillary EC in diabetic limb muscles at 14d post-ischemia induction. Values are means±SEM. *P<0.05 vs. Ad.GFP. (g) The percentage of BM-resident Sca-1⁺Lin^- progenitor cells undergoing apoptosis (recognized by Annexin-V staining) is significantly reduced by intramuscular delivery of Ad.DN-p75^NTR in diabetic mice. Values are means±SEM. ⁺P<0.05 vs. healthy with Ad.Null.*P<0.05 vs. diabetic with Ad.Null. (h) Representative examples of FACS analyses of diabetic BM are shown. First, monocytic cells were identified by size/granularity (left panel), followed by selection of Sca-1⁺Lin^- cells (R2, central panel). Finally, the percentage of cells positive for Annexin-V was calculated (R4, right panel).

Fig. 6 — Unilateral limb ischemia was induced in diabetic and normoglycemic mice before an adenovirus carrying a dominant negative mutant of p75^NTR (Ad.DN-p75^NTR) or Ad.GFP was delivered to the ischemic adductor. (a) Time-course of post-ischemic BF recovery (calculated by laser colour doppler) in diabetics and normoglycemic mice treated with Ad.DN-p75^NTR or Ad.GFP; (b) Representative laser Doppler images taken at 14d after induction of ischemia are shown. Squares include the area of interest; (c) Recovery of BF (measured by Oxford Optronic) to the ischemic adductor (expressed as the ration between BF in the ischemic to BF in the contra-lateral muscle) at 14d after ischemia induction. Values are mean±SEM. *P<0.05 vs. healthy with Ad.GFP, ^§P<0.05 versus diabetic with Ad.GFP. (d) Capillary density in the ischemic adductor at 14d post-ischemia. Values are means±SEM. **P<0.01 vs. healthy with Ad.GFP, ^§§P<0.05 vs. diabetic with Ad.GFP. (e) Apoptosis (revealed by TUNEL assay) and (f) proliferation (revealed by immunhistochemistry for the proliferation antigen MCM-2) of capillary EC in diabetic limb muscles at 14d post-ischemia induction. Values are means±SEM. *P<0.05 vs. Ad.GFP. (g) The percentage of BM-resident Sca-1⁺Lin^- progenitor cells undergoing apoptosis (recognized by Annexin-V staining) is significantly reduced by intramuscular delivery of Ad.DN-p75^NTR in diabetic mice. Values are means±SEM. ⁺P<0.05 vs. healthy with Ad.Null.*P<0.05 vs. diabetic with Ad.Null. (h) Representative examples of FACS analyses of diabetic BM are shown. First, monocytic cells were identified by size/granularity (left panel), followed by selection of Sca-1⁺Lin^- cells (R2, central panel). Finally, the percentage of cells positive for Annexin-V was calculated (R4, right panel).