Study schematic and immuno-phenotype of ASCs.

<p>Panel (a) Schematic of the <i>in vivo</i> and <i>in vitro</i> experiment. Panel (b) CD29, CD31, CD44 and CD45 were detected by flow cytometry. Results showed that the fourth passage ASCs were largely positive for CD29 (99.80±0.10%) and CD44 (99.60±0.20%), and only minority of ASCs were positive for CD31 (0.30±0.10%) and CD45 (0.45±0.10%). The expression of CXCR4 on ASCs was 9.96±0.07%.</p

Evaluation of ASCs migration and differentiation <i>in vivo</i>.

<p>Seven days after ASCs transplantation, immuno-staining analysis showed that in comparison of group blank control, the number of ASCs migrated in peri-infarcted areas was significantly increased in group Ator, however, the efficacy with atorvastatin therapy was abolished when SDF-1α up-regulation was diminished or SDF-1α/CXCR-4 coupling was blockage as shown in group A+L-NAME and A+AMD3100. (sham operated: 4.4±2.3, blank control: 13.3±2.2*, Ator: 22.6±2.9*#, A+L-NAME: 15.0±2.3*$, A+AMD3100: 14.5±2.5*$, per high power field). No significant difference was found in ASCs differentiation among each group (sham operated: 4.6±0.2%, blank control: 4.7±0.2%, Ator: 4.5±0.2%, A+L-NAME: 4.7±0.2%, A+AMD3100: 4.6±0.2%). (Scale Bar: 50 µm).</p

Comparisons of eNOS, p-eNOS, NO and SDF-1α levels in each group.

<p>Panel (a) Western-blot analysis showed that a significant increment of eNOS expression in group Ator, A+L-NAME and A+AMD3100 for <i>in vivo</i> study when compared with blank control. (sham operated: 0.28±0.07, blank control: 0.41±0.10*, Ator: 0.88±0.16*#, A+L-NAME: 0.93±0.15*#, A+AMD3100: 0.92±0.13*#). Similar changes were found in p-eNOS expression among each group (sham operated: 0.33±0.06, blank control: 0.46±0.11*, Ator: 0.93±0.14*#, A+L-NAME: 1.01±0.18*#, A+AMD3100: 0.95±0.16*#). Panel (b) Analyses of eNOS expression by Western-blot for <i>in vitro</i> study showed that as compared with group blank control, eNOS was significantly increased in group Ator, A+L-NAME and A+AMD3100. (sham operated: 0.42±0.08, blank control: 0.61±0.10*, Ator: 0.86±0.13*#, A+L-NAME: 0.89±0.11*#, A+AMD3100: 0.92±0.14*#). Similar changes were found in p-eNOS expression among each group (sham operated: 0.33±0.06, blank control: 0.50±0.09*, Ator: 0.76±0.11*#, A+L-NAME: 0.81±0.13*#, A+AMD3100: 0.78±0.10*#). Panel(c) When compared with group blank control, the NO productions <i>in vitro</i> and <i>in vivo</i> were identically and significantly increased in group Ator and A+AMD3100, whereas was abolished in group A+L-NAME. (<i>In vivo</i> study, sham operated: 6.03±1.10, blank control: 6.22±0.98, Ator: 10.31±0.86*#, A+L-NAME: 8.86±1.03*#, A+AMD3100: 11.10±0.92*#) and (in vitro study, sham operated: 3.62±0.42, blank control: 4.11±0.66, Ator: 7.03±0.71*#, A+L-NAME: 5.02±0.69*#, A+AMD3100: 7.11±0.70*#). Panel (d) As compared with group blank control, the SDF-1α expressions <i>in vitro</i> and <i>in vivo</i> was profoundly increased with atorvastatin therapy; however, the effects were reduced in group A+L-NAME. (<i>In vivo</i> study, sham operated: 5.53±0.73, blank control: 6.05±0.95, Ator: 10.88±1.33*#, A+L-NAME: 7.92±1.09*#, A+AMD3100: 9.86±1.21*#) and (in vitro study, sham operated: 3.84±0.47, blank control: 4.21±0.65, Ator: 8.12±0.77*#, A+L-NAME: 5.88±0.70*#, A+AMD3100: 7.76±0.73*#).</p

Comparison of ASCs apoptotic index <i>in vivo.</i>

<p><i> In vivo</i> apoptotic index was detected by TUNEL, and the results showed that compared with group blank control, atorvastatin therapy significantly reduced apoptotic index of ASCs, nevertheless, the efficacy was offset when either L-NAME or AMD3100 was added. (sham operated: 22.6±5.5, blank control: 52.1±9.4*, Ator: 31.3±6.7*#, A+L-NAME: 46.0±8.3*$, A+AMD3100: 49.7±7.8*$, per high power field). (Scale Bar: 50 µm).</p