Extended Data Fig. 8: Dysregulated CXCL16-S1PR1 signaling disrupts angiogenesis in the GE. | Nature Neuroscience

Extended Data Fig. 8: Dysregulated CXCL16-S1PR1 signaling disrupts angiogenesis in the GE.

From: Proinflammatory immune cells disrupt angiogenesis and promote germinal matrix hemorrhage in prenatal human brain

Extended Data Fig. 8

(a) Confocal images show expression of tight junction ZO-1 in the GE of E12.5 CTRL and Cdh5−Cre;S1pr1fl/fl mice. (b) Confocal images show similar proliferation in IBA1+ cells in the GE and CP of CTRL and Cdh5−Cre;S1pr1fl/fl mice. (c–e) Confocal images and quantification show higher abundance of CD16+ cells in the GE of E12.5 Cdh5−Cre;S1pr1fl/fl mice (c) and in the GE of GW24-25 human GMH cases (d, e), when compared to age-matched controls. CD68+ vesicle volume in IBA1+ cells remains unchanged between age-matched CTRL and GMH cases. n indicates the number of independent biological samples used for quantification. (f–h) Violin plots show upregulated (f), downregulated (g), and unchanged expressions (h) of key protein transcripts in most CD45+ cell subtypes from GMH cases, when compared to age-matched CTRL cases. Statistics in panel e use two-tailed, unpaired Student’s t-test, data represent mean ± SEM. ns, not significant. Data in panels f-h are from 2 independent biological samples in each condition (Control, GMH).

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