Publication: Perivascular PDGFRB plus cells accompany lesion formation and clinical evolution differentially in two different EAE models
dc.contributor.authorid | 0000-0002-0860-8964 | |
dc.contributor.authorid | 0000-0003-3222-874X | |
dc.contributor.authorid | 0000-0003-3413-0332 | |
dc.contributor.authorid | N/A | |
dc.contributor.authorid | 0000-0003-3672-7343 | |
dc.contributor.authorid | 0000-0001-6783-4593 | |
dc.contributor.authorid | 0000-0001-6503-8665 | |
dc.contributor.authorid | 0000-0001-8882-0019 | |
dc.contributor.authorid | 0000-0002-4292-9761 | |
dc.contributor.authorid | 0000-0001-5948-8491 | |
dc.contributor.coauthor | Ulusoy, Canan | |
dc.contributor.coauthor | Seyaj, Seddiq Zeybel, Mujdat | |
dc.contributor.coauthor | Tuncer, Asli | |
dc.contributor.coauthor | Karabudak, Rana | |
dc.contributor.coauthor | Kucukali, Cem Ismail | |
dc.contributor.coauthor | Tuzun, Erdem | |
dc.contributor.department | KUTTAM (Koç University Research Center for Translational Medicine) | |
dc.contributor.kuauthor | Özdemir, Yasemin Gürsoy | |
dc.contributor.kuauthor | Vural, Atay | |
dc.contributor.kuauthor | Çakmak, Özgür Öztop | |
dc.contributor.kuauthor | Budan, Abdullah Salih | |
dc.contributor.kuauthor | Uçar, Ege Anıl | |
dc.contributor.kuauthor | Gökyüzü, Aysu Bilge | |
dc.contributor.kuauthor | Özkan, Esra | |
dc.contributor.kuauthor | Atak, Dila | |
dc.contributor.kuauthor | Şekerdağ, Emine | |
dc.contributor.kuauthor | Köseoğlu, Gülsüm Deniz | |
dc.contributor.kuauthor | Özdemir, Yasemin Gürsoy | |
dc.contributor.kuauthor | Vural, Atay | |
dc.contributor.kuauthor | Çakmak, Özgür Öztop | |
dc.contributor.kuauthor | Budan, Abdullah Salih | |
dc.contributor.kuauthor | Uçar, Ege Anıl | |
dc.contributor.kuauthor | Gökyüzü, Aysu Bilge | |
dc.contributor.kuauthor | Özkan, Esra | |
dc.contributor.kuauthor | Atak, Dila | |
dc.contributor.kuauthor | Şekerdağ, Emine | |
dc.contributor.kuprofile | Faculty Member | |
dc.contributor.kuprofile | Faculty Member | |
dc.contributor.kuprofile | Faculty Member | |
dc.contributor.kuprofile | Undergraduate Student | |
dc.contributor.kuprofile | Undergraduate Student | |
dc.contributor.kuprofile | PhD Student | |
dc.contributor.kuprofile | Researcher | |
dc.contributor.kuprofile | PhD Student | |
dc.contributor.kuprofile | PhD Student | |
dc.contributor.kuprofile | Master Student | |
dc.contributor.yokid | 170592 | |
dc.contributor.yokid | 182369 | |
dc.contributor.yokid | 299358 | |
dc.contributor.yokid | N/A | |
dc.contributor.yokid | N/A | |
dc.contributor.yokid | N/A | |
dc.contributor.yokid | N/A | |
dc.contributor.yokid | N/A | |
dc.contributor.yokid | N/A | |
dc.contributor.yokid | N/A | |
dc.date.accessioned | 2025-01-19T10:34:15Z | |
dc.date.issued | 2023 | |
dc.description.abstract | Background: Multiple Sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) that may lead to progressive disability. Here, we explored the behavioral pattern and the role of vasculature especially PDGFRB+ pericytes/ perivascular cells, in MS pathogenesis. Methods: We have evaluated vascular changes in two different experimental allergic encephalomyelitis (EAE) mice models (MOG and PLP-induced). PDGFRB+ cells demonstrated distinct and different behavioral patterns. In both models, fibrosis formation was detected via collagen, fibronectin, and extracellular matrix accumulation. Results: The PLP-induced animal model revealed that fibrosis predominantly occurs in perivascular locations and that PDGFRB+ cells are accumulated around vessels. Also, the expression of fibrotic genes and genes coding extracellular matrix (ECM) proteins are upregulated. Moreover, the perivascular thick wall structures in affected vessels of this model presented primarily increased PDGFRB+ cells but not NG2+ cells in the transgenic NG2DsRed transgenic animal model. On the other hand, in MOG induced model, PDGFRB+ perivascular cells were accumulated at the lesion sites. PDGFRB+ cells colocalized with ECM proteins (collagen, fibronectin, and lysyl oxidase L3). Nevertheless, both MOG and PLP-immunized mice showed increasing EAE severity, and disability parallel with enhanced perivascular cell accumulation as the disease progressed from earlier (day 15) to later (day 40). Conclusion: As a result, we have concluded that PDGFRB+ perivascular cells may be participating in lesion progression and as well as demonstrating different responses in different EAE models. | |
dc.description.indexedby | WoS | |
dc.description.indexedby | Scopus | |
dc.description.indexedby | PubMed | |
dc.description.publisherscope | International | |
dc.description.volume | 69 | |
dc.identifier.doi | 10.1016/j.msard.2022.104428 | |
dc.identifier.eissn | 2211-0356 | |
dc.identifier.issn | 2211-0348 | |
dc.identifier.quartile | Q2 | |
dc.identifier.scopus | 2-s2.0-85145477212 | |
dc.identifier.uri | https://doi.org/10.1016/j.msard.2022.104428 | |
dc.identifier.uri | https://hdl.handle.net/20.500.14288/26763 | |
dc.identifier.wos | 1027788200001 | |
dc.keywords | Multiple sclerosis | |
dc.keywords | Fibrosis | |
dc.keywords | Perivascular | |
dc.keywords | Pericytes | |
dc.keywords | PDGFRB | |
dc.keywords | NG2 | |
dc.keywords | MOG | |
dc.keywords | PLP | |
dc.keywords | EAE | |
dc.language | en | |
dc.publisher | Elsevier Sci Ltd | |
dc.source | Multiple Sclerosis and Related Disorders | |
dc.subject | Clinical Neurology | |
dc.title | Perivascular PDGFRB plus cells accompany lesion formation and clinical evolution differentially in two different EAE models | |
dc.type | Journal Article | |
dspace.entity.type | Publication | |
local.publication.orgunit1 | SCHOOL OF MEDICINE | |
local.publication.orgunit1 | Graduate School of Health Sciences | |
local.publication.orgunit2 | School of Medicine | |
relation.isOrgUnitOfPublication | 91bbe15d-017f-446b-b102-ce755523d939 | |
relation.isOrgUnitOfPublication.latestForDiscovery | 91bbe15d-017f-446b-b102-ce755523d939 |