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Cerebroprotective Role of N6-Methyladenosine Demethylase FTO (Fat Mass and Obesity-Associated Protein) After Experimental Stroke.
Chokkalla, Anil K; Jeong, Soomin; Mehta, Suresh L; Davis, Charles K; Morris-Blanco, Kahlilia C; Bathula, Saivenkateshkomal; Qureshi, Simran S; Vemuganti, Raghu.
Afiliación
  • Chokkalla AK; Department of Neurological Surgery (A.K.C., S.J., S.L.M., C.K.D., K.C.M.-B., S.B., S.S.Q., R.V.), University of Wisconsin, Madison.
  • Jeong S; Department of Pathology and Immunology, Baylor College of Medicine and Texas Children's Hospital, Houston (A.K.C.).
  • Mehta SL; Department of Neurological Surgery (A.K.C., S.J., S.L.M., C.K.D., K.C.M.-B., S.B., S.S.Q., R.V.), University of Wisconsin, Madison.
  • Davis CK; Neuroscience Training Program (S.J., R.V.), University of Wisconsin, Madison.
  • Morris-Blanco KC; Department of Neurological Surgery (A.K.C., S.J., S.L.M., C.K.D., K.C.M.-B., S.B., S.S.Q., R.V.), University of Wisconsin, Madison.
  • Bathula S; Department of Neurological Surgery (A.K.C., S.J., S.L.M., C.K.D., K.C.M.-B., S.B., S.S.Q., R.V.), University of Wisconsin, Madison.
  • Qureshi SS; Department of Neurological Surgery (A.K.C., S.J., S.L.M., C.K.D., K.C.M.-B., S.B., S.S.Q., R.V.), University of Wisconsin, Madison.
  • Vemuganti R; Department of Cell & Developmental Biology, The University of Pennsylvania Perelman School of Medicine, Philadelphia (K.C.M.-B.).
Stroke ; 54(1): 245-254, 2023 01.
Article en En | MEDLINE | ID: mdl-36321453
BACKGROUND: FTO (fat mass and obesity-associated protein) demethylates N6-methyladenosine (m6A), which is a critical epitranscriptomic regulator of neuronal function. We previously reported that ischemic stroke induces m6A hypermethylation with a simultaneous decrease in FTO expression in neurons. Currently, we evaluated the functional significance of restoring FTO with an adeno-associated virus 9, and thus reducing m6A methylation in poststroke brain damage. METHODS: Adult male and female C57BL/6J mice were injected with FTO adeno-associated virus 9 (intracerebral) at 21 days prior to inducing transient middle cerebral artery occlusion. Poststroke brain damage (infarction, atrophy, and white matter integrity) and neurobehavioral deficits (motor function, cognition, depression, and anxiety-like behaviors) were evaluated between days 1 and 28 of reperfusion. RESULTS: FTO overexpression significantly decreased the poststroke m6A hypermethylation. More importantly, exogenous FTO substantially decreased poststroke gray and white matter damage and improved motor function recovery, cognition, and depression-like behavior in both sexes. CONCLUSIONS: These results demonstrate that FTO-dependent m6A demethylation minimizes long-term sequelae of stroke independent of sex.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Accidente Cerebrovascular Tipo de estudio: Risk_factors_studies Límite: Animals Idioma: En Revista: Stroke Año: 2023 Tipo del documento: Article Pais de publicación: Estados Unidos
Texto completo
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XML
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Accidente Cerebrovascular Tipo de estudio: Risk_factors_studies Límite: Animals Idioma: En Revista: Stroke Año: 2023 Tipo del documento: Article Pais de publicación: Estados Unidos