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Öğe A novel theanine complex, Mg-L-Theanine improves sleep quality via regulating brain electrochemical activity(Frontiers Media S.A., 2022) Daşdelen, Muhammed Furkan; Er, Sezgin; Kaplan, Berkan; Çelik, Süleyman; Beker, Mustafa Çağlar; Orhan, Cemal; Tuzcu, Mehmet; Şahin, Nurhan; Mamedova, Havakhanum; Sylla, Sarah; Komorowski, James; Ojalvo, Sara PerezL-Theanine is commonly used to improve sleep quality through inhibitory neurotransmitters. On the other hand, Mg2+, a natural NMDA antagonist and GABA agonist, has a critical role in sleep regulation. Using the caffeine-induced brain electrical activity model, here we investigated the potency of L-theanine and two novel Mg-L-theanine compounds with different magnesium concentrations on electrocorticography (ECoG) patterns, GABAergic and serotonergic receptor expressions, dopamine, serotonin, and melatonin levels. Furthermore, we evaluated the sleep latency and duration in the pentobarbital induced sleep model. We herein showed that L-theanine, particularly its various complexes with magnesium increases the expression of GABAergic, serotonergic, and glutamatergic receptors, which were associated with decreased ECoG frequency, increased amplitude, and enhanced delta wave powers. Besides increased dopamine, serotonin, and melatonin; decreased MDA and increased antioxidant enzyme levels were also observed particularly with Mg-complexes. Protein expression analyses also showed that Mg-L-theanine complexes decrease inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) levels significantly. In accordance with these results, Mg complexes improved the sleep latency and duration even after caffeine administration. As a result, our data indicate that Mg-L-theanine compounds potentiate the effect of L-theanine on sleep by boosting slow-brain waves, regulating brain electrical activity, and increasing neurotransmitter and GABA receptor levels.Öğe ACKR3 regulates platelet activation and ischemia-reperfusion tissue injury(Nature Research, 2022) Rohlfing, Anne-Katrin; Kolb, Kyra; Sigle, Manuel; Ziegler, Melanie; Bild, Alexander; Münzer, Patrick; Sudmann, Jessica; Dicenta, Valerie; Harm, Tobias; Manke, Mailin-Christin; Geue, Sascha; Kremser, Marcel; Chatterjee, Madhumita; Liang, Chunguang; Eysmondt, Hendrik von; Dandekar, Thomas; Heinzmann, David; Günter, Manina; Ungern-Sternberg, Saskia von; Büttcher, Manuela; Castor, Tatsiana; Mencl, Stine; Langhauser, Friederike; Sies, Katharina; Ashour, Diyaa; Beker, Mustafa Çağlar; Lämmerhofer, Michael; Autenrieth, Stella E.; Schäffer, Tilman E.; Laufer, Stefan; Szklanna, Paulina; Maguire, Patricia; Heikenwalder, Matthias; Müller, Karin Anne Lydia; Hermann, Dirk M.; Kılıç, Ertuğrul; Stumm, Ralf; Ramos, Gustavo; Kleinschnitz, Christoph; Borst, Oliver; Langer, Harald F.; Rath, Dominik; Gawaz, MeinradPlatelet activation plays a critical role in thrombosis. Inhibition of platelet activation is a cornerstone in treatment of acute organ ischemia. Platelet ACKR3 surface expression is independently associated with all-cause mortality in CAD patients. In a novel genetic mouse strain, we show that megakaryocyte/platelet-specific deletion of ACKR3 results in enhanced platelet activation and thrombosis in vitro and in vivo. Further, we performed ischemia/reperfusion experiments (transient LAD-ligation and tMCAO) in mice to assess the impact of genetic ACKR3 deficiency in platelets on tissue injury in ischemic myocardium and brain. Loss of platelet ACKR3 enhances tissue injury in ischemic myocardium and brain and aggravates tissue inflammation. Activation of platelet-ACKR3 via specific ACKR3 agonists inhibits platelet activation and thrombus formation and attenuates tissue injury in ischemic myocardium and brain. Here we demonstrate that ACKR3 is a critical regulator of platelet activation, thrombus formation and organ injury following ischemia/reperfusion.Öğe Acute and post-acute neuromodulation induces stroke recovery by promoting survival signaling, neurogenesis, and pyramidal tract plasticity(Frontiers Media Sa, 2019) Çağlayan, Ahmet Burak; Beker, Mustafa Çağlar; Çağlayan, Berrak; Yalçın, Esra; Çağlayan, Aysun; Yuluğ, Burak; Hanoğlu, Lütfü; Kutlu, Selim; Doeppner, Thorsten Roland; Hermann, Dirk Matthias; Kılıç, ErtuğrulRepetitive transcranial magnetic stimulation (rTMS) has gained interest as a non-invasive treatment for stroke based on the data promoting its effects on functional recovery. However, the exact action mechanisms by which the rTMS exert beneficial effects in cellular and molecular aspect are largely unknown. To elucidate the effects of high- and low-frequency rTMS in the acute-ischemic brain, we examined how rTMS influences injury development, cerebral blood flow (CBF), DNA fragmentation, neuronal survival, pro- and anti-apoptotic protein activations after 30 and 90 min of focal cerebral ischemia. In addition, inflammation, angiogenesis, growth factors and axonal outgrowth related gene expressions, were analyzed. Furthermore, we have investigated the effects of rTMS on post-acute ischemic brain, particularly on spontaneous locomotor activity, perilesional tissue remodeling, axonal sprouting of corticobulbar tracts, glial scar formation and cell proliferation, in which rTMS was applied starting 3 days after the stroke onset for 28 days. In the high-frequency rTMS received animals reduced DNA fragmentation, infarct volume and improved CBF were observed, which were associated with increased Bcl-xL activity and reduced Bax, caspase-1, and caspase-3 activations. Moreover, increased angiogenesis, growth factors; and reduced inflammation and axonal sprouting related gene expressions were observed. These results correlated with reduced microglial activation, neuronal degeneration, glial scar formation and improved functional recovery, tissue remodeling, contralesional pyramidal tract plasticity and neurogenesis in the subacute rTMS treated animals. Overall, we propose that high-frequency rTMS in stroke patients can be used to promote functional recovery by inducing the endogenous repair and recovery mechanisms of the brain.Öğe Age-associated resilience against ischemic injury in mice exposed to transient middle cerebral artery occlusion(Springer, 2023) Beker, Mustafa Çağlar; Aydınlı, Fatmagül İlayda; Çağlayan, Ahmet Burak; Beker, Merve; Baygül, Oğuzhan; Çağlayan, Aysun; Popa-Wagner, Aurel; Doeppner, Thorsten R.; Hermann, Dirk M.; Kılıç, ErtuğrulIschemic stroke is the leading cause of death and disability. Although stroke mainly affects aged individuals, animal research is mostly one on young rodents. Here, we examined the development of ischemic injury in young (9-12-week-old) and adult (72-week-old) C57BL/6 and BALB/c mice exposed to 30 min of intraluminal middle cerebral artery occlusion (MCAo). Post-ischemic reperfusion did not differ between young and adult mice. Ischemic injury assessed by infarct area and blood-brain barrier (BBB) integrity assessed by IgG extravasation analysis was smaller in adult compared with young mice. Microvascular viability and neuronal survival assessed by CD31 and NeuN immunohistochemistry were higher in adult than young mice. Tissue protection was associated with stronger activation of cell survival pathways in adult than young mice. Microglial/macrophage accumulation and activation assessed by F4/80 immunohistochemistry were more restricted in adult than young mice, and pro- and anti-inflammatory cytokine and chemokine responses were reduced by aging. By means of liquid chromatography-mass spectrometry, we identified a hitherto unknown proteome profile comprising the upregulation of glycogen degradation-related pathways and the downregulation of mitochondrial dysfunction-related pathways, which distinguished post-ischemic responses of the aged compared with the young brain. Our study suggests that aging increases the brain's resilience against ischemic injury.Öğe Bioenergetic shift and proteomic signature induced by lentiviral-transduction of gfp-based biosensors(2024) Barakat, Sarah; Çimen, Şeyma; Miri, Seyed Mohammad; Vatandaşlar, Emre; Yelkenci, Hayriye Ecem; San Martín, Alejandro; Beker, Mustafa Çağlar; Kök, Kıvanç; Öztürk, Gürkan; Eroğlu, EmrahFluorescent proteins (FPs) stand as pivotal tools extensively employed across diverse biological research endeavors in various model systems. However, long-standing concerns surround their use due to the numerous side effects associated with their expression. Recent investigations have brought to light the significance of hydrogen peroxide (H2O2) that is associated with the maturation process of green fluorescent protein (GFP) fluorophores. The structural and functional impairments associated with GFP expression are possibly linked to this amount of H2O2. In this study, we assess the impact of the GFP-based HyPer7 biosensor on cellular homeostasis and proteome changes, aiming to identify potential risks related to oxidative stress responses that potentially risks the application of such tools. Cells expressing genome-integrated HyPer7 demonstrated altered mitochondrial membrane potential (MMP), which was alleviated by the addition of antioxidants or culturing cells at physiological normoxia (5 kPa O2). Additionally, HyPer7-expressing cells also exhibited significant impairment in mitochondrial oxidative respiration, suggesting broader mitochondrial dysfunction. Through untargeted proteomics analysis, we identified 26 proteins exhibiting differential expression in HyPer7-expressing cells compared to respective control cells. Functional annotation analysis showed that the list of the delineated proteins is associated with cellular responses to stress and the regulation of antioxidant mechanisms. Our findings underscore the significance of caution and validation in ensuring a thorough comprehension of cellular responses when using fluorescent protein-based tools, thereby enhancing the reliability of the results.Öğe BMAl1'in beyin hasarı sonrası rolününproteomik açıdan incelenmesi(İstanbul Medipol Üniversitesi Sağlık Bilimleri Enstitüsü, 2021) Özbay, Elif; Beker, Mustafa ÇağlarSirkadiyen ritim, iç ve dış uyaranlara bağlı olarak hemen hemen tüm fizyolojik durumlarımızı kontrol eden önemli bir biyolojik saattir. Bunun yanı sıra, sirkadiyen ritmin özellikle beyin felci gibi nörodejeneratif hastalıkların görülmesinde ve bu hastalıklar sonrasında gelişen patofizyolojik süreçlerde önemli bir rolünün olduğu düşünülmektedir. Beyin felci dünyada ölüm nedenleri bakımından ikinci sırada yer alan ve kısıtlı bir tedavi imkânı bulunan bir hastalıktır. Bu nedenle beyin felci patofizyolojisini etkileyen faktörler ve uygulanabilir tedavi yöntemlerinin araştırılması, günümüzün araştırma konuları arasında yer almaktadır. Bu tez kapsamında; sirkadiyen ritmin düzenlenmesinde önemli bir rolü bulunan BMAL1 proteininin beyin hasarı sonrası hücre içi sinyal yolakları üzerine olan etkisinin proteomik araçlarla araştırılması hedeflenmiştir. Bu amaçla BMAL1 protein seviyesini arttırmak veya azaltmak için dizayn edilen lentiviral vektörler beyin içi enjeksiyon yöntemiyle 8-12 haftalık erkek C57BL/6 farelerine uygulanmıştır. Enjeksiyondan 7 gün sonra farelere 30 dakikalık orta serebral arter tıkanmasını takiben 72 saat reperfüzyon uygulanmıştır. Striatum seviyesinden alınan koronal beyin kesitlerden nöronal sağkalım ve DNA fragmantasyonu değerlendirilmiştir. Ayrıca, striatumdan alınan doku örneklerinden sıvı kromatografisi- kütle spektrometresi aracılı proteomik analizler gerçekleştirilmiştir. Elde edilen bulgulara göre, BMAL1 protein seviyesinin artmasıyla nöronal sağkalımın değişmediği fakat apoptotik hücre ölümünün baskılandığı; BMAL1 protein seviyesinin baskılanmasıyla nöronal sağkalımın azaldığı ve apoptotik hücre sayısının arttığı gösterilmiştir. Ek olarak, BMAL1 proteinin direkt veya dolaylı olarak etkileşimde bulunan 178 protein belirlenmiştir. Ayrıca BMAL1 protein seviyesinin artmasıyla 19, baskılanmasıyla 32 proteinin istatistiksel olarak anlamlı değiştiği gösterilmiştir. Elde edilen bulguların sirkadiyen ritim ve beyin felci patofizyolojisi arasındaki ilişkinin ve sinyal yolaklarının aydınlatılmasına katkı sağlaması beklenmektedir.Öğe Can Carpobrotus edulis, heal incisional and excisional wounds on the skin?(Comenius University, 2021) Günal, Mehmet Yalçın; Şahinler Ayla, Sibel; Çaglayan, Berrak; Beker, Mustafa Çağlar; Bedri, Nejda; Aslan, İpek Bilge; Özdemir, Ekrem Musa; Kılıç, Ertuğrul; Yeşilada, ElifOBJECTIVES: This study aimed to investigate the wound healing activity of liposomal Carpobrotus edulis powder extract (CEPE) formulation on incisional and excisional wounds in rat. BACKGROUND: In the event of any damage, the damaged tissue undergoes a process of regenerating itself, which is called wound healing. METHODS: Centella asiatica extract (CAE) was used as the reference molecule in the study. The wound healing process was tested by using the excisional and incisional wound model. On the 12th day of the study, maximum stress, stress, % of elongation values were evaluated in the incisional wound. Also; histological parameters and macroscopic photographic analyses were evaluated in the excisional wound. RESULTS: In the photo evaluations, the improvement was more prominent in both CAE and CEPE groups than in the control group. Histological evaluation showed that CEPE group had signifi cant wound healing activity compared to the control and CAE groups. Axial tensile-elongation experiments in incisional wound tissue show that there was no signifi cant difference between CAE and CEPE groups. CONCLUSION: Liposomal formulations of C.edulis extract were found to have positive effects on the healing process, both on excisional and incisional wound tissues (Tab. 2, Fig. 3, Ref. 30).Öğe Delayed therapeutic administration of melatonin enhances neuronal survival through AKT and MAPK signaling pathways following focal brain ischemia in mice(Springer Nature, 2022) Kılıç, Ülkan; Elibol, Birsen; Çağlayan, Ahmet Burak; Beker, Mustafa Çağlar; Beker, Merve; Altuğ Tasa, ?Burcugül; Uysal, Ömer; Yılmaz, Bayram; Kılıç, ErtuğrulMelatonin has a role in the cell survival signaling pathways as a candidate for secondary stroke prevention. Therefore, in the present study, the coordination of ipsilateral and contralateral hemispheres to evaluate delayed post-acute effect of melatonin was examined on recovery of the cell survival and apoptosis after stroke. Melatonin was administered (4 mg/kg/day) intraperitoneally for 45 days, starting 3 days after 30 min of middle cerebral artery occlusion. The genes and proteins related to the cell survival and apoptosis were investigated by immunofluorescence, western blotting, and RT-PCR techniques after behavioral experiments. Melatonin produced delayed neurological recovery by improving motor coordination on grip strength and rotarod tests. This neurological recovery was also reflected by high level of NeuN positive cells and low level of TUNEL-positive cells suggesting enhanced neuronal survival and reduced apoptosis at the fifty-fifth day of stroke. The increase of NGF, Nrp1, c-jun; activation of AKT; and dephosphorylation of ERK and INK at the fifty-fifth day showed that cell survival and apoptosis signaling molecules compete to contribute to the remodeling of brain. Furthermore, an increase in the CREB and Atf-1 expressions suggested the melatonin's strong reformative effect on neuronal regeneration. The contralateral hemisphere was more active at the latter stages of the molecular and functional regeneration which provides a further proof of principle about melatonin's action on the promotion of brain plasticity and recovery after stroke.Öğe Development of light and pH-dual responsive self-quenching theranostic SPION to make EGFR overexpressing micro tumors glow and destroy(Elsevier B.V., 2023) Verimli, Nihan; Goralı, Selen İrem; Abişoğlu, Beyza; Altan, Cem Levent; Sucu, Bilgesu Onur; Karataş, Ersin; Tülek, Ahmet; Bayraktaroğlu, Çiğdem; Beker, Mustafa Çağlar; Erdem, Sultan SibelDrug resistant and undetectable tumors easily escape treatment leading metastases and/or recurrence of the lethal disease. Therefore, it is vital to diagnose and destroy micro tumors using simple yet novel approaches. Here, we present fluorescence-based detection and light-based destruction of cancer cells that are known to be resistant to standard therapies. We developed a superparamagnetic iron oxide nanoparticle (SPION)-based theranostic agent that is composed of self-quenching light activated photosensitizer (BPD) and EGFR targeting ligand (Anti-EGFR ScFv or GE11 peptide). Photosensitizer (BPD) was immobilized to PEG-PEI modified SPION with acid-labile linker. Prior to stimulation of the theranostic system by light its accumulation within cancer cells is vital since BPD phototoxicity and fluorescence is activated by lysosomal proteolysis. As BPD is cleaved, the system switches from off to on position which triggers imaging and therapy. Targeting, therapeutic and diagnostic features of the theranostic system were evaluated in high and moderate level EGFR expressing pancreatic cancer cell lines. Our results indicate that the system distinguishes high and moderate EGFR expression levels and yields up to 4.3-fold increase in intracellular fluorescence intensity. Amplification of fluorescence signal was as low as 1.3-fold in the moderate or no EGFR expressing cell lines. Anti-EGFR ScFv targeted SPION caused nearly 2-fold higher cell death via apoptosis in high EGFR expressing Panc-1 cell line. The developed system, possessing advanced targeting, enhanced imaging and effective therapeutic features, is a promising candidate for multi-mode detection and destruction of residual drug-resistant cancer cells.Öğe Dual action of exosomes derived from in vitro A beta toxicity model: The role of age for pathological response(Elsevier Ireland Ltd, 2023) Beker, Merve; Günay, Necmeddin; Sarıkamış, Bahar; Kalkan Çakmak, Rabia; Erçin, Nilüfer; Altıntaş, Mehmet Özgen; Altunay, Serdar; Beker, Mustafa Çağlar; Sarı Ak, Duygu; Kılıç, ÜlkanExosomes released from different cell types of the central nervous system play an essential role in the patho-genesis of Alzheimer's disease (AD). In this study, we aimed to create an animal model by injecting exosomes that carry AD markers into the brain to shed light on the mechanism behind Alzheimer's pathology. Exosomes obtained from mouse Neuro2A, to which A beta toxicity model applied, were used as a mediator to build an AD phenotype. For this purpose, exosomes were administered into hippocampal CA3 region of mice with different ages. Firstly, the possible role of exosomes on brain volume was analyzed. Then, neurons and astrocytes were evaluated for survival. In addition, the progenitor cells' differentiation capacity was investigated via BrdU staining. AKT signaling pathway components were examined to detect the molecular mechanisms behind the exosomal function. We found different responses in different age groups. Expression of APP upregulated only in young animals upon delivery of A beta-exosomes. Interestingly, young animals represented increased numbers of neurons in the hippocampus, and neurogenesis was found to be restricted after A beta-Ex injections. However, in relation to exosome administration, the glial intensity increased in aged animals. Lastly, phosphorylation of survival kinase AKT was downregulated due to the presence of A beta in both young and old animals. The findings reveal that the exosomes from an in vitro A beta toxicity model may induce different responses in an age-dependent manner. This study is the first to report the relationship between exosomal function and aging by evaluating the key molecules.Öğe Effect of circadian rhythm protein BMAL1 on neuronal damage(Wiley, 2017) Beker, Mustafa Çağlar; Serel, Elif; Karaçay, Reyda; Altunay, Serdar; Dilden, Aysun; Çağlayan, Ahmet Burak; Keleştemur, Taha; Çağlayan, Berrak; Yalçın, Esra; Kılıç, Ertuğrul[Abstract Not Available]Öğe Effect of P2X7 receptor on activation of microglia and IL1 beta following ischemia(Wiley, 2017) Çağlayan, Berrak; Çağlayan, Ahmet Burak; Beker, Mustafa Çağlar; Yalçın, Esra; Beker, Merve; Keleştemur, Taha; Şahin, Fikrettin; Kılıç, Ertuğrul[Abstract Not Available]Öğe Effect of social isolation on the brain injury following focal cerebral ischemia in mice and proteomic approach for identifying possible cellular pathways(Wiley, 2021) Çağlayan, Ahmet Burak; Daşdelen, Muhammed Furkan; Beker, Mustafa Çağlar; Özbay, Erkan; Kılıç, E.Social isolation has become a significant part of our everyday life during the Covid-19 pandemic, resulting in drastic effects on physiological wellbeing. It was shown that loneliness or psychosocial stress such as social isolation, predict the onset of depression, as well as increased stroke-related morbidity and mortalityÖğe Effects of bmal1 on akt signal pathway after oxygen glucose deprivation(Wiley, 2018) Beker, Mustafa Çağlar[Abstract Not Available]Öğe Effects of circadian rhythm on brain injury and related molecular mechanisims(Wiley-Blackwell, 2016) Beker, Mustafa Çağlar; Çağlayan, Ahmet Burak; Keleştemur, Taha; Çağlayan, Berrak; Yalçın, Esra; Dalay, Arman; Altunay, Serdar; Sertel, Elif; Kılıç, Ertuğrul[Abstract Not Available]Öğe Effects of GDNF on neurovascular structures during recovery process after cerebral ischemia(Wiley, 2019) Beker, Merve; Beker, Mustafa Çağlar; Çağlayan, Ahmet Burak; Köse Torun, Gamze; Kılıç, Ertuğrul[Abstract Not Available]Öğe Effects of neurotrophic factors cdnf and manf on brain plasticity and repair after brain ischemia(Wiley-Blackwell, 2016) Çağlayan, Ahmet Burak; Beker, Mustafa Çağlar; Çağlayan, Berrak; Altunay, Serdar; Dalay, Arman; Dilden, Aysun; Sertel, Elif; Keleştemur, Taha; Yalçın, Esra; Kılıç, Ülkan; Saarma, Mart; Kılıç, Ertuğrul[Abstract Not Available]Öğe Effects of normobaric oxygen and melatonin treatment on newborn hypoxia plasiticity(Wiley, 2017) Keleştemur, Taha; Beker, Mustafa Çağlar; Çağlayan, Ahmet Burak; Çağlayan, Berrak; Dalay, Arman; Altunay, Serdar; Yalçın, Esra; Sertel, Elif; Dilden, Aysun; Kılıç, Ertuğrul[Abstract Not Available]Öğe Effects of pde10a and bmal1 on circadian rhythm and brain injury(Wiley, 2019) Beker, Mustafa Çağlar[Abstract Not Available]Öğe Effects of repetitive transcranial magnetic stimulation on motor activity and neuronal survival after spinal cord injury(Wiley, 2017) Dalay, Arman; Balçıkanlı, Zeynep; Altunay, Serdar; Keleştemur, Taha; Tancan, Emre; Çağlayan, Ahmet Burak; Beker, Mustafa Çağlar; Kılıç, Ertuğrul[Abstract Not Available]
