Person: BEKER, MERVE
29 results
Search Results
Now showing 1 - 10 of 29
Publication Metadata only Behavioral and molecular effects of perinatal music on rat pups(2016-11-16) Yanık, Hilal; CAN, BİRSEN; KIRPINAR, İSMET; BEKER, MERVE; ELİBOL, BİRSEN; KIRPINAR, İSMET; BEKER, MERVEPublication Metadata only Lentivirally administered glial cell line-derived neurotrophic factor promotes post-ischemic neurological recovery, brain remodeling and contralesional pyramidal tract plasticity by regulating axonal growth inhibitors and guidance proteins(2020-09-01T00:00:00Z) Beker, Merve; Caglayan, Ahmet B.; Beker, Mustafa C.; Altunay, Serdar; Karacay, Reyda; Dalay, Arman; Altintas, Mehmet O.; KÖSE, GAMZE; Hermann, Dirk M.; KILIÇ, ERTUĞRUL; BEKER, MERVEOwing to its potent longterm neuroprotective and neurorestorative properties, glial cell line-derived neurotrophic factor (GDNF) is currently studied in neurodegenerative disease clinical trials. However, little is known about the longterm effect of GDNF on neurological recovery, brain remodeling and neuroplasticity in the post-acute phase of ischemic stroke. In a comprehensive set of experiments, we examined the effects of lentiviral GDNF administration after ischemic stroke. GDNF reduced neurological deficits, neuronal injury, blood-brain barrier permeability in the acute phase in mice. As compared with control, enhanced motor-coordination and spontaneous locomotor activity were noted in GDNF-treated mice, which were associated with increased microvascular remodeling, increased neurogenesis and reduced glial scar formation in the peri-infarct tissue. We observed reduced brain atrophy and increased plasticity of contralesional pyramidal tract axons that crossed the midline in order to innervate denervated neurons in the ipsilesional red and facial nuclei. Contralesional axonal plasticity by GDNF was associated with decreased abundance of the axonal growth inhibitors brevican and versican in contralesional and ipsilesional brain tissue, reduced abundance of the growth repulsive guidance molecule ephrin b1 in contralesional brain tissue, increased abundance of the midline growth repulsive protein Slit1 in contralesional brain tissue and reduced abundance of Slit1-s receptor Robo2 in ipsilesional brain tissue. These data indicate that GDNF potently induces longterm neurological recovery, peri-infarct brain remodeling and contralesional neuroplasticity, which are associated with the fine-tuned regulation of axonal growth inhibitors and guidance molecules that facilitate the growth of contralesional corticofugal axons in the direction to the ipsilesional hemisphere.Publication Metadata only Association of reelin silencing and topo isomerase IIβ expression in human SH-SY5Y neuroblastoma cell line(2019-09-07) TERZİOĞLU UŞAK, ŞULE; BEKER, MERVE; ELİBOL, BİRSEN; TERZİOĞLU, ŞULE; ELİBOL, BİRSEN; BEKER, MERVEPublication Metadata only Melatonin’in phenytoin sodium’un oluşturduğu DNA hasarı üzerine etkisi(2013-09-30) gök, özlem; ERCAN, ÇİLEM; BEKER, MERVE; UYSAL, ÖMER; kılıç, ülkan; ERCAN, ÇİLEM; BEKER, MERVE; UYSAL, ÖMERPublication Metadata only Melatonin promotes neurological recovery, peri-lesional tissue remodeling, and contralesional pyramidal tract plasticity after focal cerebral ischemia(2015-10-21) kılıç, ülkan; Beker, mustafa çağlar; çağlayan, ahmet burak; ELİBOL, BİRSEN; BEKER, MERVE; altuğ, burcugül; gök, özlem; keleştemur, taha; kılıç, ertuğrul; ELİBOL, BİRSEN; BEKER, MERVEPublication Metadata only Evidence that activation of P2X7R does not exacerbate neuronal death after optic nerve transection and focal cerebral ischemia in mice(2017-10-01T00:00:00Z) Caglayan, Berrak; Caglayan, Ahmet B.; Beker, Mustafa C.; Yalcin, Esra; BEKER, MERVE; Kelestemur, Taha; Sertel, Elif; ÖZTÜRK, GÜRKAN; Kilic, Ulkan; ŞAHİN, FİKRETTİN; KILIÇ, ERTUĞRUL; BEKER, MERVEConflicting data in the literature about the function of P2X7R in survival following ischemia necessitates the conductance of in-depth studies. To investigate the impacts of activation vs inhibition of the receptor on neuronal survival as well as the downstream signaling cascades, in addition to optic nerve transection (ONT), 30 min and 90 min of middle cerebral artery occlusion (MCAo) models were performed in mice. Intracellular calcium levels were assessed in primary cortical neuron cultures. Here, we show that P2X7R antagonist Brilliant Blue G (BBG) decreased DNA fragmentation, infarct volume, brain swelling, neurological deficit scores and activation of microglial cells after focal cerebral ischemia. BBG also significantly increased the number of surviving retinal ganglion cells (RGCs) after ONT and the number of surviving neurons following MCAo. Importantly, receptor agonist BzATP resulted in increased activation of microglial cells and induced phosphorylation of ERK,AKT and JNK. These results indicated that inhibition of P2X7R with BBG promoted neuronal survival, not through the activation of survival kinase pathways, but possibly by improved intracellular Ca2+ overload and decreased the levels of Caspase 1, IL-1 beta and Bax proteins. On the other hand, BzATP-mediated increased number of activated microglia and increased survival kinase levels in addition to increased caspase-1 and IL-1 beta levels indicate the complex nature of the P2X7 receptor-mediated signaling in neuronal injury. (C) 2017 Elsevier Inc. All rights reserved.Publication Metadata only Effects of fetal alcohol and maternal intubation stress on the expression of proteins controlling postnatal development of male rat hippocampus(2020-09-01T00:00:00Z) ELİBOL, BİRSEN; BEKER, MERVE; KILIÇ, ÜLKAN; Jakubowska-Dogru, Ewa; ELİBOL, BİRSEN; BEKER, MERVEBackground Developing brains can partially get over prenatal alcohol exposure-related detrimental conditions by activating some mechanisms involved in survival. Objectives This study aimed to shed light on the molecular correlates of compensatory mechanisms by examining temporal profiles in the expression of proteins controlling postnatal development in the rat hippocampus prenatally exposed to intubation stress/ethanol. Methods Male pups were randomly assigned to age subgroups (n = 21/age) which were sacrificed on postnatal day (PD)1, PD10, PD30, and PD60. Ethanol (6 g/kg/day) were intragastrically intubated to the dams throughout 7-21 gestation days. The expression of neurogenesis and angiogenesis markers, extracellular matrix proteins, and growth-promoting ligands were examined by western blot. Results The most rapid increase in the index of neuronal maturation was noted between PD10-PD30 (p< .05). Prenatal stress caused a decrease of neurogenesis markers at birth and an increase of their expressions at PD10 and PD30 to reach control levels (p< .001). The impact of fetal-alcohol was observed as a decrease in the expression of synaptic plasticity protein versican at birth (p< .001), an increase in the synaptic repulsion protein ephrin-B2 at PD10 (p< .001), and a decrease in the maturation of BDNF at PD30 (p< .001) with a decrease in the mature neuron markers at PD30 (p< .001) and PD60 (p= .005) which were compensated with upregulation of angiogenesis and increasing brevican expression, a neuronal maturation protein (p< .001). Conclusion These data providein vivoevidence for the potential therapeutic factors related to neurogenesis, angiogenesis, and neurite remodeling which may tolerate the alcohol/stress dependent teratogenicity in the developing hippocampus.Publication Metadata only The relationship between changes in the expression of growth associated protein-43 and functional recovery of the injured inferior alveolar nerve following transection without repair in adult rats.(2017-06-01) Çağlayan, Berrak; CAGLAYAN, AHMET BURAK; BEKER, MUSTAFA CAGLAR; BEKER, MERVE; keleştemur, taha; Sertel, Elif; Yalçın, Esra; KILIC, ULKAN; Şahin, Fikrettin; BEKER, MERVEPublication Metadata only Thymoquinone administration ameliorates Alzheimer-s disease-like phenotype by promoting cell survival in the hippocampus of amyloid beta(1-42) infused rat model(2020-12-01T00:00:00Z) ELİBOL, BİRSEN; Beker, Merve; Terzioglu-Usak, Sule; Dalli, Tugce; Kilic, Ulkan; ELİBOL, BİRSEN; BEKER, MERVE; TERZİOĞLU, ŞULEBackground: Thymoquinone (TQ), a biologically active ingredient of Nigella sativa, has anti-inflammatory, antioxidative and neuroprotective properties. Therefore, it could be a good candidate in the recovery of Alzheimer-s disease (AD) pathology rather than current symptomatic reliefs.Publication Metadata only Thymoquinone activates MAPK pathway in hippocampus of streptozotocin-treated rat model(2018-03-01) Elibol, BİRSEN; Akbas, FAHRİ; dallı, Tugce; Terzioglu-Usak, ŞULE; Beker, MERVE; BEKER, MERVE; TERZİOĞLU, ŞULE; AKBAŞ, FAHRİ; ELİBOL, BİRSENStreptozotocin (STZ), a glucosamine-nitrosourea compound, produces deficiencies in learning, memory, and cognitive functions when it was administered intracerebroventricularly (i.c.v). In molecular level, increase in neuroinflammation and oxidative stress in brain, and decrease in the number of surviving neurons are the outcomes of STZ administration. Herein, we aimed to investigate the effect of thymoquinone (TQ), an anti-inflammatory, immunomodulatory and neuroprotective agent, on STZ-induced neurodegeneration in rats. For this purpose, bilateral i.c.v. injection of STZ (3 mg/kg) was given to adult female rats on days 1 and 3. TQ (20 mg/kg/day in cornoil) was administered intragastrically to rats for 15 days starting from the 15th day of STZ injection. The Morris water maze test and passive avoidance test were applied to measure the learning and memory performance of animals. Following the behavioral tests, all of the rats were sacrificed for evaluation of molecular alterations. Rats in the STZ-TQ group showed higher performance in passive avoidance test than rats in the STZ group whose memory performance declined compared to control group. The worse memory performance in STZ group was correlated with low number of surviving neurons and high number of degenerating neurons. In addition, an increase in APOE expression and a decrease in NGF expression were observed with STZ injection. Administration of TQ reversed these STZ-triggered cognitive and molecular alterations. In the present study, we observed the neuroregenerative effects of TQ by activation of JNK protein, upregulation of mir-124, and downregulation of ERK1/2 and NOS enzymes. The same ameliorative effect of TQ was also observed in the pTau protein expression. To sum up, we can say that the healing effect of TQ on STZ induced neurodegeneration opens a new door for the development of Alzheimer-s disease treatment using natural products as an adjuvant when their action mechanism was explained in detail.
- «
- 1 (current)
- 2
- 3
- »