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Fig. 5 | Stem Cell Research & Therapy

Fig. 5

From: SHP2 mutations induce precocious gliogenesis of Noonan syndrome-derived iPSCs during neural development in vitro

Fig. 5

Increased gliogenesis in NS-cerebral organoids. a Time-dependent gliogenesis of NS-cerebral organoids. Scale bar, 20 μm. b Increment of glial cells in NS-cerebral organoids. NS-cerebral organoids expressed several glial cell markers such as GFAP (panel II), GLAST (panel III), and S100β (panel IV) in cortical plate zone. MAP2 expression was analogous between WT- and NS-cerebral organoids. Scale bar, 20 μm. c Increase of CD44 + population in the NS-cerebral organoids. Percentages of CD 44+ population are represented as the mean ± SEM (n = 5). d Reduction of GFAP-positive cells by SHP2 inhibition in NS-cerebral organoids. NS-cerebral organoids were transiently incubated with a SHP2 inhibitor (10 μM PHPS1) for 7 days (28–35th day), and then further differentiated for 3 weeks. NS-cerebral organoids treated with the inhibitor exhibited reduction of GFAP-positive cells compared with the non-treated NS-cerebral organoids. Scale bar, 20 μm. e Decreased proportion of CD44+ cells by SHP2 inhibition in NS-cerebral organoids. Percentages of CD44+ population are indicated as the mean ± SEM (n = 7). p values were determined using an unpaired Student’s t test. *p < 0.05, **p < 0.01. Abbreviation: WT, wild-type; NS, Noonan syndrome; VZ, ventricular zone; CP, cortical plate; PHPS1, phenylhydrazonopyrazolone sulfonate 1

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