Figure 6
Figure 6. Blockmirs regulate edema and angiogenesis after ischemia. (A) Hindlimb blood flow expressed as a percentage of ischemic limb blood flow over nonischemic hindlimb blood flow measured 10 days after surgery. **P < .01 (n = 6-10 mice per group). The LDBF between days 0 and 7, representing the mean of 3 independent experiments. (B) The ischemic LDBF of control and CD5-2 at day 7 is represented as a percentage over non-ischemic hind-limb blood flow. CD5-2 is represented by dashed lines; controls are represented by solid lines. (C) Assessment of edema 24 hours after hindlimb ischemia for mice treated with control Blockmir (black bars, nonischemic) and CD5-2 (white bars, ischemic). The graph is expressed as a percentage of dye leakage in either the nonischemic or ischemic side of control and CD5-2–treated mice over dye leakage in nonischemic controls. The lower part of adductor muscle was taken for quantification *P < .05, **P < .01 (n = 8 per group, results pooled from 2 independent experiments). (D) Assessment of capillary density. Sections were stained for CD31. A representative area is shown for one mouse given (i) control and (ii) CD5-2. (iii) Quantification of the number of capillaries is given as the ratio of capillaries/myocytes in the ischemic limbs (n = 4-5 animals), *P < .02. (E) Sections were co-stained with CD31 (red) and VE-cadherin (green). A representative area of the ischemic region is shown for one mouse given (i) control and (ii) CD5-2. (iii) Mean pixel intensity of VE-cadherin is expressed relative to the number of capillaries, which are CD31+ (n = 4 animals), *P < .05.

Blockmirs regulate edema and angiogenesis after ischemia. (A) Hindlimb blood flow expressed as a percentage of ischemic limb blood flow over nonischemic hindlimb blood flow measured 10 days after surgery. **P < .01 (n = 6-10 mice per group). The LDBF between days 0 and 7, representing the mean of 3 independent experiments. (B) The ischemic LDBF of control and CD5-2 at day 7 is represented as a percentage over non-ischemic hind-limb blood flow. CD5-2 is represented by dashed lines; controls are represented by solid lines. (C) Assessment of edema 24 hours after hindlimb ischemia for mice treated with control Blockmir (black bars, nonischemic) and CD5-2 (white bars, ischemic). The graph is expressed as a percentage of dye leakage in either the nonischemic or ischemic side of control and CD5-2–treated mice over dye leakage in nonischemic controls. The lower part of adductor muscle was taken for quantification *P < .05, **P < .01 (n = 8 per group, results pooled from 2 independent experiments). (D) Assessment of capillary density. Sections were stained for CD31. A representative area is shown for one mouse given (i) control and (ii) CD5-2. (iii) Quantification of the number of capillaries is given as the ratio of capillaries/myocytes in the ischemic limbs (n = 4-5 animals), *P < .02. (E) Sections were co-stained with CD31 (red) and VE-cadherin (green). A representative area of the ischemic region is shown for one mouse given (i) control and (ii) CD5-2. (iii) Mean pixel intensity of VE-cadherin is expressed relative to the number of capillaries, which are CD31+ (n = 4 animals), *P < .05.

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