Stimulation of astrocyte fatty acid oxidation by thyroid hormone is protective against ischemic stroke-induced damage.

ABSTRACT: We previously demonstrated that stimulation of astrocyte mitochondrial ATP production via P2Y₁ receptor agonists was neuroprotective after cerebral ischemic stroke. Another mechanism that increases ATP production is fatty acid oxidation (FAO). We show that in primary human astrocytes, FAO and ATP production are stimulated by 3,3,5 triiodo-l-thyronine (T3). We tested whether T3-stimulated FAO enhances neuroprotection, and show that T3 increased astrocyte survival after either hydrogen peroxide exposure or oxygen glucose deprivation. T3-mediated ATP production and protection were both eliminated with etomoxir, an inhibitor of FAO. T3-mediated protection in vitro was also dependent on astrocytes expressing HADHA (hydroxyacyl-CoA dehydrogenase/3-ketoacyl-CoA thiolase/enoyl-CoA hydra

SUBMITTER: Sayre NL 

PROVIDER: S-EPMC5381439 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature