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. Author manuscript; available in PMC: 2021 Nov 26.
Published in final edited form as: Nature. 2021 Apr 28;594(7862):271–276. doi: 10.1038/s41586-021-03562-8

Extended Data Figure 8. PI3K signaling does not augment MEKK3-KLF2/4 signaling.

Extended Data Figure 8.

a, Diagram of how gain of PI3K signaling might augment CCM formation by acting upstream of MEKK3-KLF2/4 signaling in endothelial cells. b, Immunostaining for KLF4 and the endothelial cell marker PECAM1 in hindbrain sections from P6 control, Krit1BECKO, Pik3caiBECGOF, and Krit1iBECKO;Pik3caiBECGOF neonates with either a susceptible (Susc) or resistant (Res) gut microbiome is shown. White arrows indicate endothelial cell nuclear KLF4 staining. Immunofluorescence images representative of 10 tissue sections from n=4 individual animals/genotype. Control animals are either Slco1c1-Cre;Krit1fl/+ or Krit1fl/fl. Scale bars, 50 microns. c, Measurement of Klf2 and Klf4 mRNA in endothelial cells isolated from the hindbrains of P6 control, Krit1BECKO and Pik3caiBECGOF neonates. (Control, n=8; Krit1BECKO, n=6; Pik3caiBECGOF, n=8). d, Measurement of KLF2 and KLF4 mRNA in human umbilical vein endothelial cells (HUVECs) treated with the indicated siRNAs or lentiviral vectors. (n=6 individual wells/group over 2 independent experiments). Data are mean ± s.e.m. Unpaired, two-tailed Welch’s t-test.