dc.contributor.author | Daşdelen, Muhammed Furkan | |
dc.contributor.author | Çağlayan, Ahmet Burak | |
dc.contributor.author | Er, Sezgin | |
dc.contributor.author | Beker, Mustafa Çağlar | |
dc.contributor.author | Ateş, Nilay | |
dc.contributor.author | Gronewold, Janine | |
dc.contributor.author | Doeppner, Thorsten Roland | |
dc.contributor.author | Hermann, Dirk M. | |
dc.contributor.author | Kılıç, Ertuğrul | |
dc.date.accessioned | 2024-03-07T12:19:24Z | |
dc.date.available | 2024-03-07T12:19:24Z | |
dc.date.issued | 2024 | en_US |
dc.identifier.citation | Daşdelen, M. F., Çağlayan, A. B., Er, S., Beker, M. Ç., Ateş, N., Gronewold, J. ... Kılıç, E. (2024). Social isolation initiated post-weaning augments ischemic brain injury by promoting pro-inflammatory responses. Experimental Neurology, 375. https://dx.doi.org/10.1016/j.expneurol.2024.114729 | en_US |
dc.identifier.issn | 0014-4886 | |
dc.identifier.uri | https://dx.doi.org/10.1016/j.expneurol.2024.114729 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12511/12342 | |
dc.description.abstract | Social isolation is associated with poor stroke outcome, but the underlying molecular mechanisms were largely unknown. In male Balb/C mice exposed to transient middle cerebral artery occlusion (MCAo), we examined the effects of social isolation initiated post-weaning on ischemic injury, cytokine/chemokine responses and cell signaling using a broad panel of techniques that involved immunocytochemistry, cytokine/chemokine array and Western blots. Social isolation initiated post-weaning elevated infarct size, brain edema and neuronal injury in the ischemic brain tissue 3 days after MCAo, and increased microglia/ macrophage and leukocyte accumulation. In line with the increased immune cell recruitment, levels of several proinflammatory cytokines (e.g., IL-1α, IL-1β, IL-13, IL-17, TNF-α, IFN-γ), chemokines (e.g., CCL3, CCL4, CCL12, CXCL2, CXCL9, CXCL12) and adhesion molecules (i.e., ICAM-1) were increased in the ischemic brain tissue of socially isolated compared with paired housing mice, whereas levels of selected cytokines (IL-5, IL-6, IL-16) and colony-stimulating factors (G-CSF, GM-CSF) were reduced. The activity of the transcription factor nuclear factor-ĸB (NF-ĸB), which promotes cell injury via pro-inflammatory responses, was increased by social isolation, whereas that of nuclear factor erythroid related factor-2 (Nrf-2), which mediates anti-oxidative responses under oxidative stress conditions, was reduced. Our study shows that social isolation profoundly alters post-ischemic cell signaling in a way promoting pro-inflammatory responses. Our results highlight the importance of social support in preventing deleterious health effects of social isolation. | en_US |
dc.description.sponsorship | TUBA | en_US |
dc.language.iso | eng | en_US |
dc.publisher | Academic Press Inc. | en_US |
dc.rights | info:eu-repo/semantics/embargoedAccess | en_US |
dc.subject | Chemokine | en_US |
dc.subject | Cytokine | en_US |
dc.subject | Ischemic Stroke | en_US |
dc.subject | Loneliness | en_US |
dc.subject | Microglia | en_US |
dc.subject | Neuroinflammation | en_US |
dc.title | Social isolation initiated post-weaning augments ischemic brain injury by promoting pro-inflammatory responses | en_US |
dc.type | article | en_US |
dc.relation.ispartof | Experimental Neurology | en_US |
dc.department | İstanbul Medipol Üniversitesi, Rektörlük, Sağlık Bilim ve Teknolojileri Araştırma Enstitüsü | en_US |
dc.department | İstanbul Medipol Üniversitesi, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü, Tıbbi Farmakoloji Ana Bilim Dalı | en_US |
dc.department | İstanbul Medipol Üniversitesi, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Fizyoloji Ana Bilim Dalı | en_US |
dc.authorid | 0000-0003-2251-2093 | en_US |
dc.authorid | 0000-0002-6242-3709 | en_US |
dc.authorid | 0000-0001-7266-9844 | en_US |
dc.authorid | 0000-0002-9476-8488 | en_US |
dc.authorid | 0000-0002-6637-9944 | en_US |
dc.identifier.volume | 375 | en_US |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
dc.identifier.doi | 10.1016/j.expneurol.2024.114729 | en_US |
dc.institutionauthor | Daşdelen, Muhammed Furkan | |
dc.institutionauthor | Çağlayan, Ahmet Burak | |
dc.institutionauthor | Er, Sezgin | |
dc.institutionauthor | Beker, Mustafa Çağlar | |
dc.institutionauthor | Ateş, Nilay | |
dc.identifier.wosquality | Q1 | en_US |
dc.identifier.wos | Q1 | en_US |
dc.identifier.scopus | 2-s2.0-85185511954 | en_US |
dc.identifier.pmid | 38365135 | en_US |
dc.identifier.scopusquality | Q1 | en_US |