Pharmacological Inhibition of Mitochondrial Carbonic Anhydrases Protects Mouse Cerebral Pericytes from High Glucose-Induced Oxidative Stress and Apoptosis s

Diabetes-associated complications in the microvasculature of the brain are caused by oxidative stress, generated by overproduc-tion of reactive oxygen species from hyperglycemia-induced accelerated oxidative metabolism of glucose. Pericytes, essential for the viability of the microvasculature, are especially susceptible to oxidative stress. Mitochondrial carbonic anhydrases, regu-lators of the oxidative metabolism of glucose, determine the rate of reactive oxygen species production and inhibition of mitochondrial carbonic anhydrases rescues glucose-induced pericyte loss in the diabetic mouse brain. We hypothesized that high glucose induces intracellular oxidative stress and pericyte apoptosis and that inhibition of mitochondrial carbonic anhy-drases protects pericytes from oxidative stress-induced apo-ptosis. To validate our hypothesis, conditionally immortalize