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Fig. 5 | Stem Cell Research & Therapy

Fig. 5

From: New mechanism for mesenchymal stem cell microvesicle to restore lung permeability: intracellular S1P signaling pathway independent of S1P receptor-1

Fig. 5

MSC MV increased SPHK1 and intracellular S1P levels in LPS injured HLMVEC. S1P levels in HLMVEC and in the cell supernatant at were detected by ELISA. A MSC MV significantly increased S1P secretion in HLMVEC at 24 h. B However, MSC MV significantly decreased the S1P expression in the supernatant of HLMVEC at 24 h. The effect of MSC MV on S1P levels in HLMVEC and in the cell supernatant was not abolished by the addition of W123. C, D By western blotting analysis, MSC MV treatment increased SPHK1 expression in LPS injured HLMVEC, and the increase in SPHK1 was not affected by the addition of W123. Data are presented as mean ± SD, N = 4–9. *p < 0.05 versus control using ANOVA with post hoc Tukey HSD test. MSC, mesenchymal stem cell; MV, microvesicles; HLMVEC, human lung microvascular endothelial cells; SPHK1, sphingosine kinases 1; S1P, sphingosine-1-phosphate; and ANOVA, analysis of variance

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