Figure 3.
Figure 3. Contribution of bone marrow–derived EPCs to ischemia-induced neovascularization. (A) Bone marrow (BM) transplantation mice were established to assess the contribution of vasculogenesis to ischemia-induced neovascularization. In this model, BM-derived cells or EPCs can be identified by GFP or lacZ staining, respectively. A representative lacZ histologic staining in the BM transplant–recipient animals is shown (right panel). (B) FACS analysis of the bone marrow in mice receiving transplants of cells from GFP-expressing transgenic mice revealed successful reconstitution of the bone marrow at 4 weeks. The histogram on the right shows an overlay of wild-type (shaded gray), transgenic GFP (black line), and bone marrow transplant–recipient mice (green line). (C) Application of the ischemia model to mice with tie2/lacZ bone marrow showed intense β-gal expression in severely ischemic regions (left panel), while no such expression was noted in control mice receiving transplants of wild-type bone marrow (right panel). (D) Mice that had received tie2/lacZ transplants and that had undergone excisional wounding, rather than ischemic surgery, demonstrated no gross evidence of lacZ staining; tissue at 14 days after wounding is shown.

Contribution of bone marrow–derived EPCs to ischemia-induced neovascularization. (A) Bone marrow (BM) transplantation mice were established to assess the contribution of vasculogenesis to ischemia-induced neovascularization. In this model, BM-derived cells or EPCs can be identified by GFP or lacZ staining, respectively. A representative lacZ histologic staining in the BM transplant–recipient animals is shown (right panel). (B) FACS analysis of the bone marrow in mice receiving transplants of cells from GFP-expressing transgenic mice revealed successful reconstitution of the bone marrow at 4 weeks. The histogram on the right shows an overlay of wild-type (shaded gray), transgenic GFP (black line), and bone marrow transplant–recipient mice (green line). (C) Application of the ischemia model to mice with tie2/lacZ bone marrow showed intense β-gal expression in severely ischemic regions (left panel), while no such expression was noted in control mice receiving transplants of wild-type bone marrow (right panel). (D) Mice that had received tie2/lacZ transplants and that had undergone excisional wounding, rather than ischemic surgery, demonstrated no gross evidence of lacZ staining; tissue at 14 days after wounding is shown.

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