dc.creator | Trillo Contreras, José Luis | es |
dc.creator | Ramírez Lorca, Reposo | es |
dc.creator | Hiraldo González, Laura | es |
dc.creator | Sánchez Gomar, Ismael | es |
dc.creator | Galán-Cobo, Ana | es |
dc.creator | Suárez-Luna, Nela | es |
dc.creator | Sánchez de Rojas de Pedro, Eva | es |
dc.creator | Toledo Aral, Juan José | es |
dc.creator | Villadiego Luque, Francisco Javier | es |
dc.creator | Echevarría Irusta, Miriam | es |
dc.date.accessioned | 2024-01-18T14:26:08Z | |
dc.date.available | 2024-01-18T14:26:08Z | |
dc.date.issued | 2018 | |
dc.identifier.citation | Trillo Contreras, J.L., Ramírez Lorca, R., Hiraldo González, L., Sánchez Gomar, I., Galán-Cobo, A., Suárez-Luna, N.,...,Echevarría Irusta, M. (2018). Combined effects of aquaporin-4 and hypoxia produce age-related hydrocephalus. Biochimica et Biophysica Acta - Molecular Basis of Disease, 1864 (10), 3515-3526. https://doi.org/10.1016/j.bbadis.2018.08.006. | |
dc.identifier.issn | 0925-4439 | es |
dc.identifier.issn | 1879-260X | es |
dc.identifier.uri | https://hdl.handle.net/11441/153610 | |
dc.description.abstract | Aquaporin-4, present in ependymal cells, in glia limiting and abundantly in pericapillary astrocyte foot pro cesses, and aquaporin-1, expressed in choroid plexus epithelial cells, play an important role in cerebrospinal
fluid production and may be involved in the pathophysiology of age-dependent hydrocephalus. The finding that
brain aquaporins expression is regulated by low oxygen tension led us to investigate how hypoxia and elevated
levels of cerebral aquaporins may result in an increase in cerebrospinal fluid production that could be associated
with a hydrocephalic condition. Here we have explored, in young and aged mice exposed to hypoxia, whether
aquaporin-4 and aquaporin-1 participate in the development of age-related hydrocephalus. Choroid plexus,
striatum, cortex and ependymal tissue were analyzed separately both for mRNA and protein levels of aquaporins.
Furthermore, parameters such as total ventricular volume, intraventricular pressure, cerebrospinal fluid outflow
rate, ventricular compliance and cognitive function were studied in wild type, aquaporin-1 and aquaporin-4
knock-out animals subjected to hypoxia or normoxia. Our data demonstrate that hypoxia is involved in the
development of age-related hydrocephalus by a process that depends on aquaporin-4 channels as a main route
for cerebrospinal fluid movement. Significant increases in aquaporin-4 expression that occur over the course of
animal aging, together with a reduced cerebrospinal fluid outflow rate and ventricular compliance, contribute to
produce more severe hydrocephalus related to hypoxic events in aged mice, with a notable impairment in
cognitive function. These results indicate that physiological events and/or pathological conditions presenting
with cerebral hypoxia/ischemia contribute to the development of chronic adult hydrocephalus. | es |
dc.format | application/pdf | es |
dc.format.extent | 12 p. | es |
dc.language.iso | eng | es |
dc.publisher | Elsevier | es |
dc.relation.ispartof | Biochimica et Biophysica Acta - Molecular Basis of Disease, 1864 (10), 3515-3526. | |
dc.subject | AQP4 | es |
dc.subject | Hypoxia | es |
dc.subject | Aging | es |
dc.subject | Mice | es |
dc.subject | Hydrocephalus | es |
dc.subject | Cerebrospinal fluid | es |
dc.title | Combined effects of aquaporin-4 and hypoxia produce age-related hydrocephalus | es |
dc.type | info:eu-repo/semantics/article | es |
dcterms.identifier | https://ror.org/03yxnpp24 | |
dc.type.version | info:eu-repo/semantics/acceptedVersion | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.contributor.affiliation | Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica | es |
dc.relation.publisherversion | https://www.sciencedirect.com/science/article/pii/S0925443918302916?via%3Dihub | es |
dc.identifier.doi | 10.1016/j.bbadis.2018.08.006 | es |
dc.journaltitle | Biochimica et Biophysica Acta - Molecular Basis of Disease | es |
dc.publication.volumen | 1864 | es |
dc.publication.issue | 10 | es |
dc.publication.initialPage | 3515 | es |
dc.publication.endPage | 3526 | es |