Functional and anatomical evidence of cerebral tissue hypoxia in young sickle cell anemia mice.

ABSTRACT: Cerebral ischemia is a significant source of morbidity in children with sickle cell anemia; however, the mechanism of injury is poorly understood. Increased cerebral blood flow and low hemoglobin levels in children with sickle cell anemia are associated with increased stroke risk, suggesting that anemia-induced tissue hypoxia may be an important factor contributing to subsequent morbidity. To better understand the pathophysiology of brain injury, brain physiology and morphology were characterized in a transgenic mouse model, the Townes sickle cell model. Relative to age-matched controls, sickle cell anemia mice demonstrated: (1) decreased brain tissue pO₂ and increased expression of hypoxia signaling protein in the perivascular regions of the cerebral cortex; (2) elevated basal

SUBMITTER: Cahill LS 

PROVIDER: S-EPMC5363475 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature