Researcher:
Kızılırmak, Ali Burak

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PhD Student

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Ali Burak

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Kızılırmak

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Kızılırmak, Ali Burak

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2021 - 20234

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Researcher Of Publications: search.filters.isAuthorOfPublication.cdd4e142-ed8a-44ea-bd64-b42cc12c6986

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Now showing 1 - 4 of 4
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    Novel CD20+innate lymphoid cells show increased killing capacity and are related to multiple sclerosis prognosis
    (Sage Publications Ltd, 2022) Üzülmez, M.; Baytekin, I.; Esendağlı, G.; Meinl, I.; Köseoğlu, M.; Yüksel, B.; Soysal, A.; Meinl, E.; N/A; Albayrak, Özgür; Doran, Tansu; Kızılırmak, Ali Burak; Soylu, Kemal; Erdem, Haluk; Researcher; PhD Student; PhD Student; Other; Other; N/A; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); N/A; Graduate School of Health Sciences; Graduate School of Health Sciences; N/A; N/A; N/A; N/A; N/A; N/A
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    Functional properties of CD56+CD20 natural killer cells and their relationship with demyelinating disorders
    (Sage Publications Ltd, 2021) Kizilirmak, A. B.; Uzulmez, M.; Baytekin, I.; Soylu, K.; Esendagli, G.; Meinl, I.; Koseoglu, M.; Yuksel, B.; Soysal, A.; Mainl, E.; Vural, A.; N/A; N/A; N/A; N/A; N/A; Albayrak, Özgür; Doran, Tansu; Kızılırmak, Ali Burak; Kolsuz, Selin; Erdem, Halil Eren; Researcher; PhD Student; PhD Student; Teaching Faculty; Undergraduate Student; Undergraduate Student; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); N/A; Graduate School of Health Sciences; Graduate School of Health Sciences; School of Medicine; School of Medicine; N/A; N/A; N/A; English Language Center; N/A; N/A; N/A; N/A; N/A; N/A
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    Blood-brain barrier leakage and perivascular collagen accumulation precede microvessel rarefaction and memory impairment in a chronic hypertension animal model
    (Springer/Plenum Publishers, 2021) N/A; Özkan, Esra; Taş, Yağmur Çetin; Şekerdağ, Emine; Kızılırmak, Ali Burak; Taş, Ali; Yıldız, Erdost; Eser, Hale Yapıcı; Karahüseyinoğlu, Serçin; Zeybel, Müjdat; Özdemir, Yasemin Gürsoy; Researcher; Researcher; Researcher; Master Student; Researcher; PhD Student; Faculty Member; Faculty Member; Faculty Member; Faculty Member; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); N/A; School of Medicine; N/A; Graduate School of Health Sciences; N/A; Graduate School of Health Sciences; School of Medicine; School of Medicine; School of Medicine; School of Medicine; N/A; N/A; N/A; N/A; N/A; 134359; 110772; 214694; 170592
    Hypertension (HT) is one of the main causes of vascular dementia, lead to cognitive decline. Here, we investigated the relationship between cerebral microvessels, pericytes, extracellular matrix (ECM) accumulation, blood-brain barrier (BBB) breakdown, and memory impairment at mid-life in a chronic hypertension animal model. Spontaneously hypertensive rats (SHRs) (n = 20) are chosen for the model and age matched Wistar rats (n = 16) as controls. Changes in brain microvasculature and in vitro experiments are shown with immunofluorescence studies and cognition with open field, novel object recognition, and Y maze tests. There was a significant reduction in pericyte coverage in SHRs (p = 0.021), while the quantitative parameters of the cerebral microvascular network were not different between groups. on the other hand, parenchymal albumin leakage, as a Blood-brain barrier (BBB) breakdown marker, was prominent in SHRs (p = 0.023). Extracellular matrix (ECM) components, collagen type 1, 3 and 4 were significantly increased (accumulated) around microvasculature in SHRs (p = 0.011, p = 0.013, p = 0.037, respectively). Furthermore, in vitro experiments demonstrated that human brain vascular pericytes but not astrocytes and endothelial cells secreted type I collagen upon TGF beta 1 exposure pointing out a possible role of pericytes in increased collagen accumulation around cerebral microvasculature due to HT. Furthermore, valsartan treatment decreased the amount of collagen type 1 secreted by pericytes after TGF beta 1 exposure. At the time of evaluation, SHRs did not demonstrate cognitive decline and memory impairments. Our results showed that chronic HT causes ECM accumulation and BBB leakage before leading to memory impairments and therefore, pericytes could be a novel target for preventing vascular dementia.
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    Hyperglycemia with or without insulin resistance triggers different structural changes in brain microcirculation and perivascular matrix
    (Springer/Plenum Publishers, 2023) Pekmez, Murat; N/A; Özkan, Esra; Taş, Yağmur Çetin; Şekerdağ, Emine; Yiğit Alpdoğan, Buket; Shomalizadeh, Narges; Özler, Ceyda; Kesibi, Judy; Kızılırmak, Ali Burak; Eser, Hale Yapıcı; Zeybel, Müjdat; Karahüseyinoğlu, Serçin; Özdemir, Yasemin Gürsoy; Researcher; Researcher; Researcher; Researcher; PhD Student; PhD Student; Master Student; Master Student; Master Student; Faculty Member; Faculty Member; Faculty Member; Faculty Member; N/A; School of Medicine; Graduate School of Health Sciences; N/A; Graduate School of Health Science; Graduate School of Health Science; Graduate School of Health Sciences; Graduate School of Health Sciences; Graduate School of Health Sciences; School of Medicine; School of Medicine; School of Medicine; School of Medicine; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); N/A; N/A; N/A; N/A; N/A; N/A; N/A; N/A; N/A; 134359; 214694; 110772; 170592
    Both type-1 and type-2 DM are related to an increased risk of cognitive impairment, neurovascular complications, and dementia. The primary triggers for complications are hyperglycemia and concomitant insulin resistance in type-2 DM. However, the diverse mechanisms in the pathogenesis of diabetes-related neurovascular complications and extracellular matrix (ECM) remodeling in type-1 and 2 have not been elucidated yet. Here, we investigated the high fat-high sucrose (HFHS) feeding model and streptozotocin-induced type-1 DM model to study the early effects of hyperglycemia with or without insulin resistance to demonstrate the brain microcirculatory changes, perivascular ECM alterations in histological sections and 3D-reconstructed cleared brain tissues. One of the main findings of this study was robust rarefaction in brain microvessels in both models. Interestingly, the HFHS model leads to widespread non-functional angiogenesis, but the type-1 DM model predominantly in the rostral brain. Rarefaction was accompanied by basement membrane thickening and perivascular collagen accumulation in type-1 DM; more severe blood-brain barrier leakage, and disruption of perivascular ECM organization, mainly of elastin and collagen fibers' structural integrity in the HFHS model. Our results point out that the downstream mechanisms of the long-term vascular complications of hyperglycemia models are structurally distinctive and may have implications for appropriate treatment options.