Figure 6

Treatment of hDSCs modulated neurite regeneration by dural interaction of IGF1R and CXCR4 in vivo and in vitro.

(a) In representative figures of βIII-tubulin immunoreactivity for stroke rats, U-IGF1R⁺ hDSC implantation revealed significantly longer neurites extended and more neurite-bearing neurons over the penumbral areas than that of F-IGF1R⁺ hDSCs and control rats at 28 days after cerebral ischemia. Experimental rats implanted with LV-IGF1R-sh-hDSCs or LV-CXCR4-sh-hDSCs revealed no improvement of neurite regeneration. (b) In representative figures of βIII-tubulin immunoreactivity for PCCs co-cultured with hDSCs under OGD, significantly enhanced neurite length and more neurite-bearing neurons were found in U-IGF1R⁺ hDSCs co-cultured PCCs compared to that of F-IGF1R⁺ hDSCs and controls. Increased neurite length and neurite-bearing neurons were inhibited in PCC co-cultured with LV-IGF1R-sh-hDSCs or LV-CXCR4-sh-hDSCs under OGD. (c) Significantly fewer CD68⁺ cells infiltration in the peri-infarct area was noted after U-IGF1R⁺ hDSCs treatment at 3 days after stroke compared to that of F-IGF1R⁺ hDSCs and control rats. Reduction of infiltrated CD68⁺ cells was abolished in LV-IGF1R-sh-hDSCs or LV-CXCR4-sh-hDSCs-treated stroke rats. (d) Significant reduction of proinflammatory factors and increased of anti-inflammatory factors in these mRNA expression levels was found in U-IGF1R⁺ hDSC-treated rats compared to the F-IGF1R⁺ hDSCs and control rats. In contrast, decreased proinflammatory factors and increased of anti-inflammatory factors were inhibited in the LV-IGF1R-sh-hDSC- and LV-CXCR4-sh-hDSC-treated rats. n = 8 in each group, Data are expressed as mean ± SEM. *P < 0.05 and **P < 0.01 vs. control, Bar = 40 μm.