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Cell Journal، جلد ۱۵، شماره Suppl ۱، صفحات ۴۸-۴۸
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عنوان انگلیسی Ps-69: Effects of Ecstasy in Self-Renewal Properties Mediated with Glutamate Receptor in Mouse Embryonic Stem Cells
چکیده انگلیسی مقاله Objective: Ecstasy or methylenedioxymethamphetamine (MDMA) is a potent psychomimetic drug. It is well established that this compound is neurotoxic both in vivo and in vitro. One of the purposed mechanisms for this toxicity is a secondary release of glutamate. Glutamate induces its neurotoxicity through mGlu5 receptors. In recent decades embryonic stem cell lines were used to examine pharmacological and toxicological effects of drugs in vitro and it has been reported that mGlu5 is the only glutamate receptor expressed in mESCs (mouse embryonic stem cells) and plays a role in maintenance and self-renewal properties of mESCs. In this study aims to investigate whether ecstasy could influence self-renewal via the mGlu5 receptor in mESCs Materials and Methods: In this exprimental study, we used immunocytochemistry and reverse transcriptionpolymerase chain reaction (RT-PCR) to determine the presence of the mGlu5 receptor in mESCs. The stemness characteristic in treated mESCs by immunofluorescence and flow cytometry was studied. Oneway ANOVA or repeated measure of ANOVA according to the experimental design was used for statistical analyses. Results: In this study mGlu5 expression was shown in mESCs. ecstasy (450 μM) induced a significant increment in self-renewal properties in mESCs but did not reverse 2-methyl-6(phenylethynyl) pyridine (MPEP, 1 μM), a non-competitive selective mGlu5 antagonist. Conclusion: We reported a binary role for ecstasy on mESCs; it reduced mESCs proliferation while maintaining its self- renewal. Pharmacological blockade of the mGlu5 receptor with MPEP before addition of ecstasy only partially reduced this effect. This suggests that ecstasy mediated its role trough a different mechanism, which requires further investigation. In conclusion, despite being toxic, ecstasy maintains stemness characteristics.
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نشانی اینترنتی http://celljournal.org/journal/article/abstract/873
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