Angiogenin in the Neurogenic Subventricular Zone After Stroke

Ischemic stroke is a leading cause of death and disability worldwide with effective acute thrombolytic treatments. However, brain repair mechanisms related to spontaneous or rehabilitation-induced recovery are still under investigation, and little is known about the molecules involved. The present s...

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Detalles Bibliográficos
Autores: Gabriel Salazar, Marina|||0000-0002-7521-1502, Lei, Ting|||0000-0002-2787-5208, Grayston, Alba|||0000-0002-1466-0099, Costa, Carme|||0000-0001-9577-3839, Medina-Gutiérrez, Esperanza, Comabella López, Manuel|||0000-0002-2373-6657, Montaner, Joan|||0000-0003-4845-2279, Rosell Novel, Anna|||0000-0003-1082-3599
Tipo de recurso: artículo
Fecha de publicación:2021
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:ddd.uab.cat:256490
Acceso en línea:https://ddd.uab.cat/record/256490
https://dx.doi.org/urn:doi:10.3389/fneur.2021.662235
Access Level:acceso abierto
Palabra clave:Stroke
Angiogenin
Neural stem/progenitor cells
Neurogenesis
Neurorepair
Exercise
Descripción
Sumario:Ischemic stroke is a leading cause of death and disability worldwide with effective acute thrombolytic treatments. However, brain repair mechanisms related to spontaneous or rehabilitation-induced recovery are still under investigation, and little is known about the molecules involved. The present study examines the potential role of angiogenin (ANG), a known regulator of cell function and metabolism linked to neurological disorders, focusing in the neurogenic subventricular zone (SVZ). Angiogenin expression was examined in the mouse SVZ and in SVZ-derived neural stem cells (NSCs), which were exposed to exogenous ANG treatment during neurosphere formation as well as in other neuron-like cells (SH-SY5Y). Additionally, male C57Bl/6 mice underwent a distal permanent occlusion of the middle cerebral artery to study endogenous and exercise-induced expression of SVZ-ANG and neuroblast migration. Our results show that SVZ areas are rich in ANG, primarily expressed in DCX+ neuroblasts but not in nestin+NSCs. In vitro, treatment with ANG increased the number of SVZ-derived NSCs forming neurospheres but could not modify SH-SY5Y neurite differentiation. Finally, physical exercise rapidly increased the amount of endogenous ANG in the ipsilateral SVZ niche after ischemia, where DCX-migrating cells increased as part of the post-stroke neurogenesis process. Our findings position for the first time ANG in the SVZ during post-stroke recovery, which could be linked to neurogenesis.