Person: CABADAK, HÜLYA
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CABADAK
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HÜLYA
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Publication Metadata only Studies on the role of alpha 7 nicotinic acetylcholine receptors in K562 cell proliferation and signaling(SPRINGER, 2021) AYDIN OMAY, BANU; Narin, Gozde Onder; Aydin, Banu; Cabadak, HulyaThe results we obtained from this study gave information about the determination of alpha 7 nicotinic acetylcholine receptor (alpha 7-nACh) expression in human erythroleukemia cells, as well as whether it has a role in calcium release and cell proliferation in the presence of nicotinic agonist, antagonists. Determining the roles of alpha 7 nicotinic receptors in erythroleukemia cells will also contribute to leukemia-related signal transduction studies. This study is primarily to determine the role of nicotinic agonists and antagonists in cell proliferation, alpha 7 nicotinic acetylcholine receptor expression, and calcium release. The aim of this study, which is a continuation and an important part of our previous studies on the cholinergic system, has contributed to the literature on the human erythroleukemia cell signaling mechanism. Cell viability was evaluated by the trypan blue exclusion test and Bromodeoxyuridine/5-Bromo-2 '-deoxyuridine (BrdU) labeling. Acetylcholine, nicotinic alpha 7 receptor antagonist methyllycaconitine citrate, and cholinergic antagonist atropine were used to determine the role of alpha 7-nACh in K562 cell proliferation. In our experiments, the fluorescence spectrophotometer was used in Ca2+ measurements. The expression of nicotinic alpha 7 receptor was evaluated by western blot. The stimulating effect of acetylcholine in K562 cell proliferation was reversed by both the alpha 7 nicotinic antagonist methyllycaconitine citrate and the cholinergic antagonist, atropine. Methyllycaconitine citrate inhibited K562 cell proliferation partially explained the roles of nicotinic receptors in signal transduction. While ACh caused an increase in intracellular Ca2+, methyllycaconitine citrate decreased intracellular Ca2+ level in K562 cell. The effects of nicotinic agonists and/or antagonists on erythroleukemic cells on proliferation, calcium level contributed to the interaction of nicotinic receptors with different signaling pathways. Proliferation mechanisms in erythroleukemic cells are under the control of the alpha 7 nicotinic acetylcholine receptor via calcium influx and different signalling pathway.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 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.