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The aim of this study is to investigate the role of\n DEC<\/jats:styled-content>\n 1 in 1\u2010methyl\u20104\u2010phenyl\u20101,2,3,6\u2010tetrahydropyridine (\n MPP<\/jats:styled-content>\n +<\/jats:sup>\n )\u2010induced\n PD<\/jats:styled-content>\n model.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n The location of\n DEC<\/jats:styled-content>\n 1 and tyrosine hydroxylase (\n TH<\/jats:styled-content>\n )\u2010positive neurons were detected by immunofluorescence. 1\u2010methyl\u20104\u2010phenyl\u20101,2,3,6\u2010tetrahydropyridine (\n MPTP<\/jats:styled-content>\n )\u2010induced mouse subacute model of\n PD<\/jats:styled-content>\n was established to evaluate the change of\n DEC<\/jats:styled-content>\n 1 expression in midbrain. Then,\n SH<\/jats:styled-content>\n \u2010\n SY<\/jats:styled-content>\n 5Y cells were used to investigate the role of\n DEC<\/jats:styled-content>\n 1 in\n MPP<\/jats:styled-content>\n +<\/jats:sup>\n \u2010induced neurotoxicity.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n We showed that the co\u2010expressed\n DEC<\/jats:styled-content>\n 1 and\n TH<\/jats:styled-content>\n neurons took up more than 80% of the expressed\n TH<\/jats:styled-content>\n neurons in the midbrain of mice.\n DEC<\/jats:styled-content>\n 1\/\n TH<\/jats:styled-content>\n double\u2010positive neurons decreased by 40.6% in\n SN<\/jats:styled-content>\n pc and 28.8% in\n VTA<\/jats:styled-content>\n of\n MPTP<\/jats:styled-content>\n \u2010injured mice. Consistently,\n DEC<\/jats:styled-content>\n 1,\n TH<\/jats:styled-content>\n and dopamine transporter (\n DAT<\/jats:styled-content>\n ) expression decreased in the midbrain of\n MPTP<\/jats:styled-content>\n mice. In\n SY<\/jats:styled-content>\n \u2010\n SY<\/jats:styled-content>\n 5Y cells,\n MPP<\/jats:styled-content>\n +<\/jats:sup>\n significantly suppressed\n DEC<\/jats:styled-content>\n 1 expression and increased the cleaved caspase 3\/caspase 3 and Bax\/Bcl\u20102.\n DEC<\/jats:styled-content>\n 1 overexpression relieved, whereas\n DEC<\/jats:styled-content>\n 1 knockdown aggravated\n MPP<\/jats:styled-content>\n +<\/jats:sup>\n \u2010induced cytotoxicity. Likewise,\n DEC<\/jats:styled-content>\n 1 overexpression and knockdown inversely regulated the expression of \u03b2\u2010catenin and\n PI<\/jats:styled-content>\n 3Kp110\u03b1 (\n PIK<\/jats:styled-content>\n 3\n CA<\/jats:styled-content>\n ), an essential role in Wnt\/\u03b2\u2010catenin and\n PI<\/jats:styled-content>\n 3K\/Akt signaling pathways. Interestingly,\n LY<\/jats:styled-content>\n 294002, an inhibitor of\n PI<\/jats:styled-content>\n 3K\/Akt signaling, aggravated, whereas LiCl, an activator of Wnt\/\u03b2\u2010catenin signaling, abolished the reduction in\n DEC<\/jats:styled-content>\n 1 by\n MPP<\/jats:styled-content>\n +<\/jats:sup>\n . It is established that these two pathways are interconnected by the phosphorylation status of\n GSK<\/jats:styled-content>\n 3\u03b2.\n DEC<\/jats:styled-content>\n 1 overexpression increased but\n MPP<\/jats:styled-content>\n +<\/jats:sup>\n and\n DEC<\/jats:styled-content>\n 1 knockdown decreased\n GSK<\/jats:styled-content>\n 3\u03b2 phosphorylation.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusion<\/jats:title>\n \n Downregulation of\n DEC<\/jats:styled-content>\n 1 contributes to\n MPP<\/jats:styled-content>\n +<\/jats:sup>\n \u2010induced neurotoxicity by suppressing\n PI<\/jats:styled-content>\n 3K\/Akt\/\n GSK<\/jats:styled-content>\n 3\u03b2 pathway.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/cns.12717","type":"journal-article","created":{"date-parts":[[2017,7,22]],"date-time":"2017-07-22T00:16:41Z","timestamp":1500682601000},"page":"736-747","source":"Crossref","is-referenced-by-count":19,"title":["Downregulation of\n DEC<\/scp>\n 1 contributes to the neurotoxicity induced by\n MPP<\/scp>\n +<\/sup>\n by suppressing\n PI<\/scp>\n 3K\/Akt\/\n GSK<\/scp>\n 3\u03b2 pathway"],"prefix":"10.1111","volume":"23","author":[{"given":"Zhu","family":"Zhu","sequence":"first","affiliation":[{"name":"Department of pharmacology Nanjing Medical University Nanjing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu\u2010Wen","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of pharmacology Nanjing Medical University Nanjing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ding\u2010Hao","family":"Ge","sequence":"additional","affiliation":[{"name":"Department of pharmacology Nanjing Medical University Nanjing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ming","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of pharmacology Nanjing Medical University Nanjing 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