Person: BEKER, MERVE
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Publication 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 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 Effect of P2X7 Receptor on Activation of Microglia and IL1 beta Following Ischemia(2017-09-01T00:00:00Z) Caglayan, Berrak; Caglayan, Ahmet Burak; Beker, Mustafa Caglar; Yalcin, Esra; BEKER, MERVE; Kelestemur, Taha; ŞAHİN, FİKRETTİN; KILIÇ, ERTUĞRUL; BEKER, MERVEPublication Metadata only Effects of GDNF on Neurovascular Structures During Recovery Process After Cerebral Ischemia(2019-12-01T00:00:00Z) BEKER, MERVE; Beker, Mustafa Caglar; Caglayan, Ahmet Burak; KÖSE, GAMZE; KILIÇ, ERTUĞRUL; BEKER, MERVE