Person: AYDIN OMAY, BANU
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AYDIN OMAY
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Publication Open Access The behavioral and neurochemical effects of methylprednisolone or metyrapone in a post-traumatic stress disorder rat model(KARE PUBL, 2019) AYDIN OMAY, BANU; Tanriverdi, Ayse Melek; Aydin, Banu; Bebitoglu, Berna Terzioglu; Cabadak, Hulya; Goren, M. ZaferOBJECTIVE: Mechanisms contributing to the post-traumatic stress disorder (PTSD) that involve several physiological sys- tems, and the activation of the hypothalamic-pituitary-adrenal axis (HPA) is one of the most known systems in the PTSD pathophysiology. The present study investigates the potential effects of methylprednisolone, metyrapone and their association with the noradrenergic system within the rostral pons, a region containing the locus coeruleus (LC) in a rat model of PTSD induced with predator scent. METHODS: In this study, Sprague-Dawley rats were exposed to the stress by exposure to the scent of dirty cat litter, which is a natural stressor of a predator. One week later, the rats were re-exposed to a situational reminder (clean cat litter). The rats were treated using either methylprednisolone, metyrapone or physiological saline before exposure to a situational reminder (n=8 in each group). Noradrenaline (NA) levels in the rostral pons homogenates were analysed using ELISA. RESULTS: The anxiety indices of the rats exposed to the trauma were found to be significantly higher than the anxiety indices of the control rats. Metyrapone produced a significant increase in the anxiety indices of the non-stressed rats, and methylprednisolone did not produce a change in the anxiety indices of the non-stressed rats. Methylprednisolone treatment suppressed the anxiety in the stressed rats. Metyrapone treatment increased the anxiety indices in the stressed rats but still being lower than that of the saline-treated stressed rats. Significant decrease in the freezing time was observed following the methylprednisolone treatment both in the stressed and non-stressed rats. NA content in the rostral pons of the stressed rats was significantly higher than that of the non-stressed rats. Methylprednisolone or metyrapone treatments decreased the NA content in the non-stressed rats as compared to the saline treatment. However, these decreases were not significant. CONCLUSION: In this study, findings suggest that stress may give rise to endocrine, autonomic and behavioural responses. The anxiety indices and NA levels in the rostral pons increased with the traumatic event. The methylprednisolone treatment may suppress anxiety through interactions between the LC and the HPA axis.Publication Metadata only Contribution of M-1 and M-2 muscarinic receptor subtypes to convulsions in fasted mice treated with scopolamine and given food(ELSEVIER SCIENCE BV, 2019) AYDIN OMAY, BANU; Bacanak, Merve Saygi; Aydin, Banu; Cabadak, Hulya; Nurten, Asiye; Goren, Mehmet Zafer; Enginar, NurhanTreatment of fasted mice and rats with the nonselective muscarinic antagonist, scopolamine or atropine, causes convulsions after food intake. This study evaluated the effect of fasting on the expression of M-1 and M-2 muscarinic receptors in the brain regions, the relationship between receptor expression and seizure stages, and the muscarinic receptor subtype which plays a role in the occurrence of convulsions. Mice were grouped as allowed to eat ad lib (fed) and deprived of food for 24 h (fasted). Fasted animals developed convulsions after being treated with scopolamine (60%) or the selective M-1 receptor antagonist pirenzepine (10 mg/kg; 20% and 60 mg/kg; 70%) and given food. Fasting increased expression of M-1 receptors in the frontal cortex and M-2 receptors in the hippocampus, but produced no change in the expression of both receptors in the amygdaloid complex. Food intake after fasting decreased M-1 receptor expression in the frontal cortex and M-1 and M-2 receptor expression in the hippocampus. Seizure severity was uncorrelated with muscarinic receptor expression in the brain regions. Taken together, these findings provide evidence for the role of M-1 muscarinic receptor antagonism and fasting-induced increases in M-1 and M-2 expression possible underlying mechanism in the occurrence of convulsions in fasted animals.Publication Metadata only The role of intracellular pathways in the proliferation of human K562 cells mediated by muscarinic receptors(PERGAMON-ELSEVIER SCIENCE LTD, 2013) AYDIN OMAY, BANU; Aydin, Banu; Kan, Beki; Cabadak, HulyaMuscarinic acetylcholine receptors (mAChRs) are members of the superfamily of G protein coupled receptors (GPCRs). Muscarinic receptors are relatively abundant in the central nervous system and in the peripheral parasympathetic nervous system. Several studies have suggested that muscarinic receptors also mediate some cellular events in hematopoietic cells. K562 erythroleukemia cells contain muscarinic receptors M-2, M-3 and M-4, and activation of muscarinic receptors changes cell proliferation. We examined the effects of several compounds on cell proliferation in K562 erythroleukemia cells. These included a muscarinic receptor agonist carbachol (CCh), a protein kinase inhibitor staurosporine; the phospholipase C inhibitor U73122, the MEK 1-2 inhibitor UO126, the PI3-kinase inhibitor wortmannin, the Ca2+ chelators BAPTA/AM and 2-aminoethoxy-diphenylborate (2APB). In addition, we also investigated muscarinic receptor mediated protein kinase C (PKC) expression in K562 cells. CCh caused a decrease in DNA synthesis in K562 cells supplemented with 1% fetal bovine serum after starvation. Pre-treatment of K562 cells with U73122 and BAPTA/AM antagonized the inhibitory effect of CCh, suggesting that phospholipase C and intracellular calcium are involved in CCh-mediated inhibition of proliferation in K562 cells. Our data also suggest that the regulatory roles of protein kinase C and the MAPK/ERK pathways in K562 cell proliferation are independent of cholinergic activation. (C) 2013 Elsevier Ltd. All rights reserved.Publication Metadata only Increased Noradrenaline Levels in the Rostral Pons can be Reversed by M1 Antagonist in a Rat Model of Post-traumatic Stress Disorder(SPRINGER/PLENUM PUBLISHERS, 2013) AYDIN OMAY, BANU; Terzioglu, Berna; Kaleli, Melisa; Aydin, Banu; Ketenci, Sema; Cabadak, Hulya; Goren, M. ZaferThe dysregulation of hypothalamic-pituitary-adrenal axis and noradrenergic, serotonergic and glutamatergic systems are thought to be involved in the pathophysiology of post-traumatic stress disorder. The effect of selective M1 muscarinic receptor antagonist, pirenzepine on anxiety indices was investigated by using elevated plus maze, following exposure to trauma reminder. Upon receiving the approval of ethics committee, Sprague-Dawley rats were exposed to dirty cat litter (trauma) for 10 min and 1 week later, the rats confronted to a trauma reminder (clean litter). The rats also received intraperitoneal pirenzepine (1 or 2 mg/kg/day) or saline for 8 days. Noradrenaline (NA) concentration in the rostral pons was analyzed by HPLC with electrochemical detection. The anxiety indices of the rats subjected to the trauma reminder were increased when compared to control rats (p < 0.05). Pirenzepine treatment in traumatized rats displayed similar anxiety indices of non-traumatized rats treated with physiological saline. Although freezing time was prolonged with pirenzepine in traumatized groups the change was not found statistically significant. The NA level was 1.5 +/- A 0.1 pg/mg in non-traumatized rats and increased to 2.4 +/- A 0.2 pg/mg in traumatized rats. Bonferroni post hoc test revealed that the NA content of the rostral pons of the traumatized rats treated with physiological saline was significantly higher than the content of other groups (p < 0.01). We conclude that NA content in the rostral pons increases in respect to confrontation to a trauma reminder which can be reversed by M1 antagonist pirenzepine indicating the roles of M1 receptors.Publication Open Access The role of Glu N1 activated nitric oxide synthase in rat model of post traumatic stress disorder(2016-01-01) AYDIN OMAY, BANU; CABADAK, HÜLYA; GÖREN, MEHMET ZAFER; ayhan B. G., AYKAÇ A., gür k., AYDIN B., Seçgin E., Seven İ., CABADAK H., GÖREN M. Z.Objectives: Activation of neuronal nitric oxide synthase (nNOS) and interrelated alterations of calmodulin and ionotropic glutamate receptor (GluN1) levels are unknown in post traumatic stress disorder (PTSD). Materials and Methods: Sprague-Dawley rats of both sexes were exposed to to dirty cat litter, and then placed on an elevated plus maze. An anxiety index was calculated and tissue samples from hippocampus and amygdala were prepered in order to to detect calmodulin, NOS and GluN1 by immunoblotting. Results: The anxiety indices of the traumatized rats were markedly higher than those of the controls (p<0.05). GluN1 and calmodulin levels were decreased in the dorsal hippocampus and amygdaloid complex of the traumatized rats. NOS expression increased significantly in both the amygdaloid complex and dorsal hippocampus where the increase was statistically more prominent in the amygdaloid complex (p< 0.001) than in the dorsal hippocampus of the traumatized rats (p<0.05). Conclusion: Predator exposure in rats causes long-lasting anxiogenic effects associated with increases in NOS and decreases in GluN1 expressions in brain areas related to PTSD symptoms and excitotoxicity. The results suggest that excitotoxicity occurs through other mechanisms rather than GluN1 receptors. Keywords: Predator scent test, nNOS, Glutamate, Calmodulin, Amygdala, HippocampusPublication Open Access Effects of carbachol on apoptosis in human chronic myelogenous leukemic K562 cell line(MARMARA UNIV, FAC MEDICINE, 2019-01-31) AYDIN OMAY, BANU; Aydin, Banu; Tulunay, Aysin; Eksioglu-Demiralp, Emel; Kan, Beki; Cabadak, HulyaObjectives: Muscarinic receptors mediate diverse actions of acetylcholine in the central nervous system and in non-nervous tissues innervated by the parasympathetic nervous system. Our study aims to evaluate the potential association of the M-3 muscarinic receptor with K562 cell proliferation and death. Materials and Methods: Cell proliferation was evaluated by bromodeoxyuridine (BrDU) incorporation. To show early, late apoptosis and cell death, cells were labelled with Annexin V, propidium iodide (PI) and analyzed by flow cytometry. Nuclear extracellular signal-regulated kinase (ERK/pERK) expression was measured by western blot analysis. Results: Treatment with carbachol (CCh) for 48h decreased cell number. Exposing K562 cells to CCh for 24h decreased the number of early apoptotic cells but did not change the number of late apoptotic and necrotic cells. CCh treatment for 48h increased the number of necrotic cells, but decreased the number of early and late apoptotic cells. In response to CCh, nuclear ERK expression was increased and this effect was reversed by 1,1-dimethyl-4-diphenylacetoxypiperidinium iodide (4DAMP). Nuclear pERK expression was decreased in CCh treated cells, 4DAMP did not reverse the effect. Conclusion: Our data suggest that cholinergic agonist CCh affects cell proliferation in K562 cells not only through muscarinic receptors but also through other cholinergic receptors.Publication Metadata only The change in muscarinic receptor subtypes in different brain regions of rats treated with fluoxetine or propranolol in a model of post-traumatic stress disorder(ELSEVIER SCIENCE BV, 2012) AYDIN OMAY, BANU; Aykac, Asli; Aydin, Banu; Cabadak, Hulya; Goren, M. ZaferThis study shows the possible contribution of muscarinic receptors in the pathophysiology of post-traumatic stress disorder. Sprague-Dawley rats of both sexes were exposed to dirty cat litter (trauma) for 10 min and the protocol was repeated 1 week later with a trauma reminder (clean litter). The rats also received intraperitoneal fluoxetine (2.5, 5 or 10 mg/kg/day), propranolol (10 mg/kg/day) or saline for 7 days between two exposure sessions. Functional behavioral experiments were performed using elevated plus maze, following exposure to trauma reminder. Western blot analyses for M-1, M-2, M-3, M-4 and M-5 receptor proteins were employed in the homogenates of the hippocampus, the frontal cortex and the amygdaloid complex. The anxiety indices increased from 0.63 +/- 0.02 to 0.89 +/- 0.04 in rats exposed to the trauma reminder. The freezing times were also recorded as 47 +/- 6 and 133 +/- 12 s, in control and test animals respectively. Fluoxetine or propranolol treatments restored the increases in the anxiety indices and the freezing times. Female rats had higher anxiety indices compared to males. Western blot data showed increases in M-2 and M-5 expression in the frontal cortex. Expression of M-1 receptors increased and M-4 subtype decreased in the hippocampus. In the amygdaloid complex of rats, we also detected a down-regulation of M-4 receptors. Fluoxetine and propranolol only corrected the changes occurred in the frontal cortex. These results may imply that muscarinic receptors are involved in this experimental model of post-traumatic stress disorder. (C) 2012 Elsevier B.V. All rights reserved.Publication Open Access Effects of cholinergic compounds and TNF-alpha on human erythroleukemia K562 cell proliferation and caspase expression(MARMARA UNIV, FAC MEDICINE, 2019-01-31) AYDIN OMAY, BANU; Kanli, Zebra; Aydin, Banu; Cabadak, HulyaObjective: The purpose of this study was to investigate if stimulating auto-paracrine muscarinic receptor signalling pathway could change human erythroleukemia K562 cell proliferation and caspase 3, 8 and 9 expression levels. To better understand the role of muscarinic receptors in cell signalling mechanism, we investigated the effects of several compounds on human erythroleukemia K562 cell proliferation and caspase 3, 8 and 9 expression. These compounds were M-3 muscarinic receptor agonist, pilocarpine, pro-inflammatory cytokine, tumor necrosis factor (TNF)-alpha, and the wortmannin which is a phosphoinositide 3-kinase inhibitor. Materials and Methods: Cell proliferation and cell viability were evaluated by the trypan blue exclusion test and 5-Bromo-2-deoxy-uridine (BrdU) Labelling and Detection Kits. Caspase 3, 8 and 9 expression levels were determined by immunoblot analysis. Results: Both pilocarpine and TNF-alpha caused a small increase in human erythroleukemia K562 cell proliferation. However, when all the compounds were treated together, proliferation of human erythroleukemia K562 cells increased significantly when compared to untreated control cells. TNF-alpha and wortmannin treatment increased caspase 3 and caspase 8 expression patterns significantly in human erythroleukemia K562 cells. TNF-alpha and wortmannin treatment increased caspase 9 expression level (P>0.05) but it was not significant. Conclusion: These findings partly demonstrated that M-3 muscarinic receptor mediated an increase in K562 cell proliferation. Pilocarpine prevented TNF-alpha and wortmannin induced caspase 3 and 8 expression and indirectly showed apoptosis in human erythroleukemia K562 cells.Publication Metadata only Investigation of the Roles of Non-neuronal Acetylcholine in Chronic Myeloid Leukemic Cells and their Erythroid or Megakaryocytic Differentiated Lines(BENTHAM SCIENCE PUBL LTD, 2018) AYDIN OMAY, BANU; Aydin, Banu; Cabadak, Hulya; Goren, M. ZaferBackground: Many studies suggested that Acetylcholine (ACh) might serve as an autocrine/paraerine growth factor in several types of tumors or tumor cell lines. High levels of Acetylcholinesterase (AChE) activity have been reported in primary brain tumors, ovarian, colon and lung tumors. Objectives: The role of cholinergic signaling needs to be clarified in in leukemia. Method: K562 cells were derived from a chronic myelogenous leukemia patient during blast crisis serving as pluripotent hematopoietic stein cells. K562 cells were incubated with various cholinergic agonists or antagonists to investigate the role of ACh in different differentiated cell lines. Results: Our experiments showed that AChE activity was increased in response to ACh in undifferentiated K562 cells, but in the erythroid differentiated K562 cells a high concentration of ACh (1 mM) decreased the AChE activity. ACh failed to elevate the AChE activity in the megakaryocytic differentiated K562 cells. An AChE inhibitor, eserine, also suppressed the AChE activity in a concentration-dependent manner. Choline uptake inhibition by hemicholinium did increase the AChE activity but not in the erythroid differentiated K562 DOS cell line. Likewise, megakaryocytic differentiated K562 cells also displayed a similar pattern. Vesamicole, a vesicular choline uptake inhibitor, produced similar results. Curare, a nicotinic antagonist, elevated the cell counts of the megakaryocytic differentiated cells. Conclusion: Our findings may suggest excess extracellular ACh will decrease the cell growth in undifferentiated and megakaryocytic differentiated K562 cell lines through nicotinic type cholinoceptors.Publication Metadata only Regulation of M-2, M-3, and M-4 muscarinic receptor expression in K562 chronic myelogenous leukemic cells by carbachol(INFORMA HEALTHCARE, 2011) AYDIN OMAY, BANU; Cabadak, Hulya; Aydin, Banu; Kan, BekiContext: Muscarinic receptors mediate a variety of cellular responses to acetylcholine, including inhibition of adenylate cyclase, breakdown of phosphoinositide and modulation of ion channels. These receptors are relatively abundant in the central nervous system and peripheral parasympathetic nervous system. Many cells express a mixture of muscarinic receptor transcripts. Changes in muscarinic M-2 and M-3 receptor mRNA levels in response to agonist treatment have been reported in cerebellar granule cells, Chinese hamster ovary cells, lymphocytes and in the human neuroblastoma cell line SH-SY5Y. Objective: In this study, we investigated the effects of agonist stimulation on cell proliferation and on the levels of muscarinic receptor expression in K562 chronic myelogenous leukemia cells. Methods:Total RNA and crude membrane fractions were prepared from K562 cells challenged with carbachol (CCh). Muscarinic receptor subtype expression was determined by RT-PCR and western blot analysis. Proliferation and cell viability were evaluated by the trypan blue exclusion test and BrDU labeling. Results: We showed that CCh-treatment leads to changes in muscarinic M-2, M-3, and M-4 receptor transcripts as well as M-2 and M-3 protein levels. We also found that CCh decreased proliferation of K562 cells in a time dependent manner, an effect prevented by atropine. These results suggest that CCh modulates K562 chronic myelogenous leukemic cells proliferation through muscarinic acetylcholine receptors.