Increased postischemic brain injury in mice deficient in uracil-DNA glycosylase
J. Clin. Invest. Matthias Endres, et al. 113:1711 doi:10.1172/JCI20926 [
Go to this article.]
Figure 5Effects of focal-brain ischemia in Ung
–/–, Ung
+/–, and Ung
+/+ littermate mice. (
A) Brain lesion volume and (
B) lesion areas in
Ung–/– mice compared with
Ung+/– and
Ung+/+ WT littermate mice after 30 minutes of MCAo and 72 hours of reperfusion. Brain lesion areas were determined on five anterior-posterior serial coronal H&E-stained cryostat sections (20 ∝m); mean ± SEM of 10 to 15 animals per group; **
P < 0.01, ***
P < 0.005, ANOVA and Tukey
post hoc test. (
C) Typical H&E-stained 20 ∝m brain sections from
Ung–/– and
Ung+/+ littermate mice. Scale bar: 3 mm. (
D) Neurological sensory-motor deficits were determined after 72 hours and scored from 0 (no deficit) to 3 (severe); *
P < 0.05, ANOVA on ranks (Kruskall Wallis). (
E) The development of left and right posterior communicating arteries (PcomA) was determined in carbon black_perfused brains as follows: 0, absent; 1, present but poorly developed (hypoplastic); and 2, well formed; mean ± SEM from eight animals per group; ANOVA on ranks (Kruskall Wallis). (
F) The distance from midline of the line of anastomoses between the ACA and the MCA was determined in carbon black_perfused brains; mean ± SEM from eight animals per groups. ANOVA and Tukey post hoc test.
