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Tlr2 Gene Deletion Delays Retinal Degeneration in Two Genetically Distinct Mouse Models of Retinitis Pigmentosa

dc.contributor.authorSánchez Cruz, Alonso
dc.contributor.authorCanto Méndez, Andrea
dc.contributor.authorLizasoaín Hernández, Ignacio
dc.contributor.authorde la Villa, Pedro
dc.contributor.authorRosa, Enrique J. De La
dc.contributor.authorHernández Sánchez, Catalina
dc.date.accessioned2023-06-17T08:25:19Z
dc.date.available2023-06-17T08:25:19Z
dc.date.issued2021-06-22
dc.description.abstractAlthough considered a rare retinal dystrophy, retinitis pigmentosa (RP) is the primary cause of hereditary blindness. Given its diverse genetic etiology (>3000 mutations in >60 genes), there is an urgent need for novel treatments that target common features of the disease. TLR2 is a key activator of innate immune response. To examine its role in RP progression we characterized the expression profile of Tlr2 and its adaptor molecules and the consequences of Tlr2 deletion in two genetically distinct models of RP: Pde6brd10/rd10 (rd10) and RhoP23H/+ (P23H/+) mice. In both models, expression levels of Tlr2 and its adaptor molecules increased in parallel with those of the proinflammatory cytokine Il1b. In rd10 mice, deletion of a single Tlr2 allele had no effect on visual function, as evaluated by electroretinography. However, in both RP models, complete elimination of Tlr2 attenuated the loss of visual function and mitigated the loss of photoreceptor cell numbers. In Tlr2 null rd10 mice, we observed decreases in the total number of microglial cells, assessed by flow cytometry, and in the number of microglia infiltrating the photoreceptor layers. Together, these results point to TLR2 as a mutation-independent therapeutic target for RP.en
dc.description.departmentDepto. de Farmacología y Toxicología
dc.description.departmentDepto. de Medicina
dc.description.facultyFac. de Medicina
dc.description.refereedTRUE
dc.description.sponsorshipMinisterio de Economía, Comercio y Empresa (España)
dc.description.sponsorshipInstituto de Salud Carlos III/Fondo Europeo de Desarrollo Regional
dc.description.sponsorshipComunidad de Madrid
dc.description.statuspub
dc.eprint.idhttps://eprints.ucm.es/id/eprint/71682
dc.identifier.citationSánchez Cruz, A., Canto Méndez, A., Lizasoaín Hernández, I. et al. «Tlr2 Gene Deletion Delays Retinal Degeneration in Two Genetically Distinct Mouse Models of Retinitis Pigmentosa». International Journal of Molecular Sciences, vol. 22, n.o 15, julio de 2021, p. 7815. DOI.org (Crossref), https://doi.org/10.3390/ijms22157815.
dc.identifier.doi10.3390/ijms22157815
dc.identifier.issn1422-0067
dc.identifier.officialurlhttps://doi.org/10.3390/ijms22157815
dc.identifier.relatedurlhttps://www.mdpi.com/1422-0067/22/15/7815/htm
dc.identifier.urihttps://hdl.handle.net/20.500.14352/7056
dc.issue.number15
dc.journal.titleInternational Journal of Molecular Sciences
dc.language.isoeng
dc.page.initial7815
dc.publisherMPDI
dc.relation.projectID(SAF2016-75681-R and PID2019-109506RB-100)
dc.relation.projectID(RETICS-FEDER RD16/0008/0020; FIS/PI18-00754; PI20/00535; RETICS RD16/0019/0009 )
dc.relation.projectIDMULTI-TARGET&VIEW-CM (B2017/BMD-3688)
dc.rightsAtribución 3.0 España
dc.rights.accessRightsopen access
dc.rights.urihttps://creativecommons.org/licenses/by/3.0/es/
dc.subject.keywordRetinitis pigmentosa
dc.subject.keywordRetina
dc.subject.keywordTLR
dc.subject.keywordTLR2
dc.subject.keywordMicroglia
dc.subject.keywordInnate immunity
dc.subject.keywordNeurodegeneration
dc.subject.keywordrd10
dc.subject.keywordP23H
dc.subject.ucmGenética médica
dc.subject.ucmÓptica y optometría
dc.subject.ucmBaja visión
dc.subject.unesco2410.07 Genética Humana
dc.subject.unesco2209 Óptica
dc.subject.unesco2209.24 Física de la visión
dc.titleTlr2 Gene Deletion Delays Retinal Degeneration in Two Genetically Distinct Mouse Models of Retinitis Pigmentosaen
dc.typejournal article
dc.volume.number22
dspace.entity.typePublication
relation.isAuthorOfPublicatione02a31a0-06d8-4949-bfb8-95ae7ac4d1b9
relation.isAuthorOfPublication22bd5da1-89a4-434c-8dca-7c2f8db2b710
relation.isAuthorOfPublication.latestForDiscoverye02a31a0-06d8-4949-bfb8-95ae7ac4d1b9

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