Hypoxia-Inducible Factor-1? Is Associated With Sprouting Angiogenesis in the Murine Laser-Induced Choroidal Neovascularization Model

Basit Öğe Kaydı
dc.contributor.authorAndre, Helder
dc.contributor.authorTunik, Selcuk
dc.contributor.authorAronsson, Monica
dc.contributor.authorKvanta, Anders
dc.date.accessioned2024-04-24T17:14:31Z
dc.date.available2024-04-24T17:14:31Z
dc.date.issued2015
dc.departmentDicle Üniversitesien_US
dc.description.abstractPURPOSE. To investigate the expression and distribution of neoangiogenic molecules and the role of hypoxia during the development of experimental choroidal neovascularization (CNV). METHODS. Lesions were induced on C57Bl6 mice using laser photocoagulation. Animals were euthanized in a timely manner and eyecups were dissected from enucleated eyes. Choroids were immunostained for pericytes, sprouting endothelial cells (EC), or vascular EC. Choroidal neovascularization lesions where analyzed for tissue hypoxia, hypoxia-inducible factors (HIF), and heat-shock proteins (HSP). RESULTS. Choroidal neovascularization lesions showed a trend of increased cellular recruitment throughout the time-course and the lesions displayed positive staining for angiogenic markers. Both pericytes and sprouting EC displayed a radial progression, while vascular EC displayed a more uniform distribution across the CNV lesions. Furthermore, positive tissue hypoxia staining was observed and associated with expression of HIF-1 alpha and vascular endothelial growth factor (VEGF). CONCLUSIONS. Our data delimitate specific temporal windows during CNV initiation, propagation, maturation, and even recovery in experimental CNV. We show that murine CNV undergoes hypoxia-associated sprouting angiogenesis, and demonstrate involvement of pericytes. Moreover, we have shown expression of HIF-1 alpha to the retinal pigment epithelium surrounding the CNV lesions, together with VEGF upregulation, independently of the HSP response induced by the laser thermal insult.en_US
dc.identifier.doi10.1167/iovs.15-16476
dc.identifier.endpage6604en_US
dc.identifier.issn0146-0404
dc.identifier.issn1552-5783
dc.identifier.issue11en_US
dc.identifier.pmid26501235
dc.identifier.scopus2-s2.0-84945263445
dc.identifier.scopusqualityQ1
dc.identifier.startpage6591en_US
dc.identifier.urihttps://doi.org/10.1167/iovs.15-16476
dc.identifier.urihttps://hdl.handle.net/11468/18021
dc.identifier.volume56en_US
dc.identifier.wosWOS:000368235100051
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherAssoc Research Vision Ophthalmology Incen_US
dc.relation.ispartofInvestigative Ophthalmology & Visual Science
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectAge-Related Macular Degenerationen_US
dc.subjectAngiogenesisen_US
dc.subjectAnimal Modelsen_US
dc.subjectChoroidal Neovascularizationen_US
dc.subjectHypoxiaen_US
dc.subjectHypoxia-Inducible Factorsen_US
dc.titleHypoxia-Inducible Factor-1? Is Associated With Sprouting Angiogenesis in the Murine Laser-Induced Choroidal Neovascularization Modelen_US
dc.titleHypoxia-Inducible Factor-1? Is Associated With Sprouting Angiogenesis in the Murine Laser-Induced Choroidal Neovascularization Model
dc.typeArticleen_US

Dosyalar

Koleksiyon

WoS İndeksli Yayınlar Koleksiyonu
PubMed İndeksli Yayın Koleksiyonu
Scopus İndeksli Yayınlar Koleksiyonu