Fig. 5: ApoM-S1P-S1PR1 signaling promotes SVZ-NSCs self-renewal via ERK pathway and inhibits BMP2 expression. | Nature Communications

Fig. 5: ApoM-S1P-S1PR1 signaling promotes SVZ-NSCs self-renewal via ERK pathway and inhibits BMP2 expression.

From: HDL-bound S1P affects the subventricular niche and early neuropathological features of Alzheimer’s disease

Fig. 5

a Quantification of the number and diameter of neurospheres after treatment with ApoM-HDL and ApoM+HDL in NSCs derived from wild-type SVZ (left to right, n  = 9, 4, 4, 4). b A Venn diagram illustrating the DEGs of SVZ-NSCs in a comparison as indicated. c Heatmap of expression values for DEGs. d GO term enrichment analysis of biological process using DAVID Bioinformatics Resources 6.8. e Western blot analysis of p-ERK, p-p38, p-JNK, and p-AKT levels in SVZ-NSCs treated with ApoM+HDL, including comparisons of pretreatment with or without W146, and PTX (n  =  4/group). f Quantification of the number of neurospheres following treatment with ApoM+HDL, with additional comparisons for pretreatment with or without W146, PTX, and U0126 (n  =  8/group). g GO term enrichment analysis of cellular component using DAVID Bioinformatics Resources 6.8. h Hub genes identified from the PPI network using the Cytohubba plug in Cytosacpe. i mRNA levels of BMP2 in SVZ-NSCs after treatment with ApoM-HDL and ApoM+HDL (n  =  5/group). j Representative immunofluorescence images and quantification of BMP2 immunoreactivity in the SVZ of WT, Apom-/- and Apom-/- mice transplanted with Apom-/- or ApomTG serum (n  =  5/group). Scale bars, 30 μm. k Quantification of BMP2 immunoreactivity in the SVZ of WT, S1pr1ΔGFAP; Apom-/- mice and S1pr1ΔGFAP; Apom-/- mice transplanted with Apom-/- or ApomTG serum (n  =  5/group). a, e, f, j, k One-way analysis of variance, Tukey’s post hoc test. d, e One-sided Fisher’s exact test with Benjamini-Hochberg correction for multiple testing. i Two-tailed student’s t test. All error bars indicate s.e.m. Source data are provided as a Source Data file.

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