PMC:4608092 / 45105-46769 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/4608092","sourcedb":"PMC","sourceid":"4608092","source_url":"https://www.ncbi.nlm.nih.gov/pmc/4608092","text":"Figure 18 Suppressive effect of Rnf213 mutant upregulation in ECs on angiogenesis in vivo. A, Representative images of GLUT-1-stained sections of cerebral cortex of EC-Mut Tg, EC-WT Tg, SMC-Mut Tg, KO, and WT mice under conditions of normoxia (N) and hypoxia (H). B, Quantified result of cerebral microvessels (left panel). A column with a bar represents mean±SD of the number of cerebral microvessels/mm2 from 6 mice per group. In the hypoxia condition, there was a significant difference in the number of cerebral microvessels among 5 genotypes using the nonparametric method, Kruskal–Wallis 1-way ANOVA (P=0.036), but not in the normoxia condition (P=0.41). *P\u003c0.05 according to Mann–Whitney U test compared with normoxia condition. Two-way ANOVA method was conducted for microvessel formation between genotypes and treatment with interaction term. Results and parameter estimates are described in table (right panel). Regression models are described as (microvessels)=(intercept)+α×[Genotype: EC-Mut-Tg]+β×[Genotype: EC-WT-Tg]+γ×[Genotype: SMC-Mut-Tg]+δ×[Genotype: KO]+ε×[Treatment]+ζ×[interaction: EC-Mut-Tg]+η×[interaction: EC-WT-Tg]+θ×[interaction: SMC-Mut-Tg]+ι×[interaction: KO]. Treatment (hypoxia) significantly induced the number of microvessels/mm2 (P\u003c0.001), whereas genotype did not (P=0.09). Interaction between genotype and treatment was significant (P=0.02). The coefficient on EC-Mut-Tg (ζ) was negative, suggesting that this genotype did not increase microvessels (P=0.002). #P\u003c0.05 according to 2-way ANOVA. ECs indicates endothelial cells; GLUT-1, glucose transporter; KO, knockout; SMC, smooth muscle cells; Tg, transgenic; WT, wild type.\nF","tracks":[]}