FIG. 6.

Proangiogenic response and mobilization of PACs are disrupted in Nrf2^−/− mice. (A, B) 500,000 of PACs (Nrf2^+/+ or Nrf2^−/−) were mixed with Matrigel and injected subcutaneously at the ventral side of GFP transgenic mice. At day 15 the percentage of endothelial cells defined as (A) GFP⁺/CD45⁻/CD31⁺ and (B) GFP⁻/CD45⁻/CD31⁺ was determined in the Matrigel plugs. Flow cytometry (n_Nrf2+/+=8; n_Nrf2−/−=10). (C–F) Nrf2^+/+ and Nrf2^−/− mice were subjected to FAL. Preoperatively (untreated) and at days 1 and 3 after surgery, the percentage of the progenitors defined as CD45⁻/Sca-1⁺ and CD45⁻/Sca-1⁺/lectin⁺ was determined in the bone marrow (C, D) (n_Nrf2+/+=8; n_Nrf2−/−=6–8) and peripheral blood (E, F) (n_Nrf2+/+=10–12; n_Nrf2−/−=10–11). Flow cytometry. (G, H) SDF-1α gradient in response to FAL is impaired in Nrf2^−/− mice. The ratio of SDF-1α expression at the mRNA level (RT-PCR) in caput gastrocnemius (G) (n_Nrf2+/+=8–11; n_Nrf2−/−=9–10) and adductor (H) (n_Nrf2+/+=5–8; n_Nrf2−/−=6–8) muscles to the mRNA level of SDF-1α in the bone marrow; each bar represents the mean±SEM. *p<0.05, untreated versus ischemia (appropriate time point), ^#p<0.05, Nrf2^+/+ versus Nrf2^−/−. FAL, femoral artery ligation.