Extended Data Figure 5 : The Slco1c1(BAC)-CreERT2 transgene is selectively expressed in brain endothelial cells and confers CCM formation when used to drive deletion of Krit1 in neonatal mice.

From: Endothelial TLR4 and the microbiome drive cerebral cavernous malformations

Extended Data Figure 5

a, R26-LSL-RFP, Cdh5(PAC)-CreERT2-R26-LSL-RFP and Slco1c1(BAC)-CreERT2-R26-LSL-RFP neonates were induced with tamoxifen injection on P1+2 (two total doses). Immunostaining for RFP and PECAM was performed at P10 in the indicated tissues. Results are representative of at least three animals per group and three independent experiments. Scale bars, 100 μm. Note the presence of RFP+PECAM+ cells in the brain, small intestine, caecum, colon and liver of Cdh5(PAC)-CreERT2-R26-LSL-RFP animals, but only in the brain of Slco1c1(BAC)-CreERT2-R26-LSL-RFP animals. b, Visual (top) and corresponding microCT (bottom) images of brains from susceptible Slco1c1(BAC)-CreERT2-Krit1fl/+ and Slco1c1(BAC)-CreERT2-Krit1fl/fl P10 animals. Arrow indicates CCM lesions in the cerebrum. Scale bars, 1 mm. c, H&E staining of cerebellum (hindbrain) from the indicated animals (left). H&E staining of cerebrum (forebrain) from the indicated animals (middle). KLF4 and PECAM immunostaining from the indicated animals (right). Scale bars, 50 μm. Asterisks denote CCM lesions. n ≥ 5 per group.