Fig. 4.

HCT 1026 increases the therapeutic efficacy of mesoangioblasts. α-SG-null mice, either untreated or exposed to a 3-month therapy with HCT 1026, were injected into the right femoral artery with GFP-expressing D16 mesoangioblasts treated or not with SDF-1. (A) Mesoangioblast migration to right (R) and left (L) gastrocnemius muscles (Gs) and liver (Li), lung (Lu), kidney (Ki), and spleen (Sp) evaluated by real-time PCR with specific primers for GFP on five animals per group. (B–E) Engrafting of mesoangioblasts to muscles. (B) Engrafting to the right and left quadriceps (Qd), Gs, and soleus (So) muscles evaluated by real-time PCR with specific primers for α-SG on three animals per group. (C) Western blot analysis of α-SG expression in Qd compared with that of GAPDH. The results shown are from one of three reproducible experiments. (D) Immunostaining of α-SG expressed in Qd fibers that were revealed in serial sections by staining with laminin; DAPI was used to identify nuclei. The results shown are from one of five reproducible experiments. (E) Specific tension of single muscle fibers (n = 101) of Gs from three animals per group. (F and G) Serum creatine kinase levels (F) and animal performance on the exhaustion treadmill tests (G), carried out as described in Fig. 1 on five animals per group. (E–G) Untreated indicates the values observed in α-SG-null mice which were neither treated with HCT 1026 nor injected with mesoangioblasts. (A, B, E–G) Bars represent SEM. Asterisks indicate statistical significance vs. α-SG-null mice injected with untreated mesoangioblasts analyzed in parallel as control (P < 0.05). wt, wild-type. [Scale bar (D), 200 μM.]