dc.creator | Netti, Vanina | es |
dc.creator | Fernández, Juan | es |
dc.creator | Melamud, Luciana | es |
dc.creator | García Miranda, Pablo | es |
dc.creator | Di Giusto, Gisela | es |
dc.creator | Ford, Paula | es |
dc.creator | Echevarría Irusta, Miriam | es |
dc.creator | Capurro, Claudia | es |
dc.date.accessioned | 2023-12-29T11:13:34Z | |
dc.date.available | 2023-12-29T11:13:34Z | |
dc.date.issued | 2021-07 | |
dc.identifier.citation | Netti, V., Fernández, J., Melamud, L., García Miranda, P., Di Giusto, G., Ford, P.,...,Capurro, C. (2021). Aquaporin-4 removal from the plasma membrane of human muller cells by AQP4-IgG from patients with neuromyelitis optica induces changes in cell volume homeostasis: the first step of retinal injury?. Cellular and Molecular Neurobiology, 58 (10), 5178-5193. https://doi.org/10.1007/s12035-021-02491-x. | |
dc.identifier.issn | 0272-4340 | es |
dc.identifier.issn | 1573-6830 | es |
dc.identifier.uri | https://hdl.handle.net/11441/152863 | |
dc.description.abstract | Aquaporin-4 (AQP4) is the target of the specifc immunoglobulin G autoantibody (AQP4-IgG) produced in patients with
neuromyelitis optica spectrum disorders (NMOSD). Previous studies demonstrated that AQP4-IgG binding to astrocytic
AQP4 leads to cell-destructive lesions. However, the early physiopathological events in Müller cells in the retina are poorly
understood. Here, we investigated the consequences of AQP4-IgG binding to AQP4 of Müller cells, previous to the infammatory response, on two of AQP4’s key functions, cell volume regulation response (RVD) and cell proliferation, a process
closely associated with changes in cell volume. Experiments were performed in a human retinal Müller cell line (MIO-M1)
exposed to complement-inactivated sera from healthy volunteers or AQP4-IgG positive NMOSD patients. We evaluated
AQP4 expression (immunofuorescence and western blot), water permeability coefcient, RVD, intracellular calcium levels
and membrane potential changes during hypotonic shock (fuorescence videomicroscopy) and cell proliferation (cell count
and BrdU incorporation). Our results showed that AQP4-IgG binding to AQP4 induces its partial internalization, leading to
the decrease of the plasma membrane water permeability, a reduction of swelling-induced increase of intracellular calcium
levels and the impairment of RVD in Müller cells. The loss of AQP4 from the plasma membrane induced by AQP4-IgG
positive sera delayed Müller cells’ proliferation rate. We propose that Müller cell dysfunction after AQP4 removal from the
plasma membrane by AQP4-IgG binding could be a non-infammatory mechanism of retinal injury in vivo, altering cell
volume homeostasis and cell proliferation and consequently, contributing to the physiopathology of NMOSD. | es |
dc.description.sponsorship | Universidad de Buenos Aires, Argentina - UBA-SECYT, 20020130100682BA, 2018–2021 | es |
dc.description.sponsorship | Agencia Nacional de Promoción Científica y Tecnológica, Argentina - ANPCyT 2019–01707 | es |
dc.description.sponsorship | Ministerio de Economía y Competitividad de España, Instituto de Salud Carlos III (ISCIII) de España y Fondo Europeo de Desarrollo Regional - FEDER, PI16/00493 | es |
dc.format | application/pdf | es |
dc.format.extent | 16 p. | es |
dc.language.iso | eng | es |
dc.publisher | Springer | es |
dc.relation.ispartof | Cellular and Molecular Neurobiology, 58 (10), 5178-5193. | |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject | Aquaporin 4 | es |
dc.subject | AQP4-IgG | es |
dc.subject | Human Müller cells | es |
dc.subject | Cell volume regulation | es |
dc.subject | Cell proliferation | es |
dc.title | Aquaporin-4 removal from the plasma membrane of human muller cells by AQP4-IgG from patients with neuromyelitis optica induces changes in cell volume homeostasis: the first step of retinal injury? | 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 | es |
dc.relation.projectID | UBA-SECYT, 20020130100682BA, 2018–2021 | es |
dc.relation.projectID | ANPCyT 2019–01707 | es |
dc.relation.projectID | FEDER, PI16/00493 | es |
dc.relation.publisherversion | https://doi.org/10.1007/s12035-021-02491-x | es |
dc.identifier.doi | 10.1007/s12035-021-02491-x | es |
dc.journaltitle | Cellular and Molecular Neurobiology | es |
dc.publication.volumen | 58 | es |
dc.publication.issue | 10 | es |
dc.publication.initialPage | 5178 | es |
dc.publication.endPage | 5193 | es |
dc.contributor.funder | Universidad de Buenos Aires (UBA). Argentina | es |
dc.contributor.funder | Agencia Nacional de Promoción Científica y Tecnológica. Argentina | es |
dc.contributor.funder | Ministerio de Economía y Competitividad (MINECO). España | es |
dc.contributor.funder | Instituto de Salud Carlos III. España | es |
dc.contributor.funder | European Commission (EC). Fondo Europeo de Desarrollo Regional (FEDER) | es |