Figure 2. Effect of global regulator of G‐protein signaling 5 (RGS5) deletion on cerebral injury after transient middle cerebral artery occlusion (MCAO).

A, Coronal brain sections of control transgenic mice expressing Cre recombinase under the control of the phosphoglycerate kinase 1 promoter (Pgk‐Cre) and global Rgs5 deficient (Rgs5 ^−/−) mice stained with 2,3,5, triphenyltetrazolium chloride (left panel) with corresponding quantification of cerebral infarct volume (right panel) (n=10). Neurological deficit score (B), sensorimotor impairment (C), brain edema formation (n=10) (D), and Evans blue leakage (E) in Pgk‐Cre (Control) and global Rgs5 ^−/− mice 24 hours after MCAO (n=5). Bar=1 mm. Quantification of blood‐brain barrier (BBB) permeability (F) and microscopic visualization of fluorescein isothiocyanate (FITC)–labeled dextran 40 kDa leakage (G), 24 hours after MCAO in Pgk‐Cre (Control) and global Rgs5 ^−/− mice (n=6). Bar=50 μm. H, BBB permeability for sodium‐FITC and 5 kDa dextran–Cascade Blue of sham operated animals (n=5). For comparisons between 2 groups, the Welch t test was used. For brain edema formation, and BBB permeability data sets, 2‐way ANOVA (variables, ipsilateral vs contralateral and Pgk‐Cre vs Rgs5 ^–/–) was conducted followed by post hoc Tukey tests. The χ² test was used for neurological deficit score data. *P<0.01.