Functional repression of cAMP response element in 6-hydroxydopamine-treated neuronal cells.

The Journal of Biological Chemistry
Elisabeth M ChalovichCharleen T Chu

Abstract

Impaired survival signaling may represent a central mechanism in neurodegeneration. 6-Hydroxydopamine (6-OHDA) is an oxidative neurotoxin used to injure catecholaminergic cells of the central and peripheral nervous systems. Although 6-OHDA elicits phosphorylation of several kinases, downstream transcriptional effects that influence neuronal cell death are less defined. The cAMP response element (CRE) is present in the promoter sequences of several important neuronal survival factors. Treatment of catecholaminergic neuronal cell lines (B65 and SH-SY5Y) with 6-OHDA resulted in repression of basal CRE transactivation. Message levels of CRE-driven genes such as brain-derived neurotrophic factor and the survival factor Bcl-2 were decreased in 6-OHDA-treated cells, but message levels of genes lacking CRE sequences were not affected. Repression of CRE could be reversed by delayed treatment with cAMP several hours after initiation of 6-OHDA injury. Furthermore, restoration of CRE-driven transcription was associated with significant neuroprotection. In contrast to observations in other model systems, the mechanism of CRE repression did not involve decreased phosphorylation of its binding protein CREB. Instead, total CREB and phospho-CRE...Continue Reading

References

Jan 15, 1982·Biochemical Pharmacology·E Tiffany-CastiglioniJ R Perez-Polo
Mar 31, 1999·Proceedings of the National Academy of Sciences of the United States of America·M YamadaD J Fink
Jun 9, 2000·Annual Review of Neuroscience·J L Goldberg, B A Barres
Aug 10, 2000·The American Journal of Pathology·K L Jordan-SciuttoC A Wiley
Oct 14, 2000·Experimental Neurology·D W HowellsG A Donnan
Jul 10, 2001·The Journal of Biological Chemistry·V Sée, J P Loeffler
Aug 3, 2001·Nature Reviews. Molecular Cell Biology·B Mayr, M Montminy
Feb 16, 2002·Methods : a Companion to Methods in Enzymology·K J Livak, T D Schmittgen
Sep 13, 2002·American Journal of Physiology. Lung Cellular and Molecular Physiology·Tim D OurySimon C Watkins
Dec 6, 2002·The American Journal of Pathology·Jian-Hui ZhuCharleen T Chu
Feb 25, 2003·The Journal of Biological Chemistry·William Andrew Holtz, Karen Laurel O'Malley
May 2, 2003·Proceedings of the National Academy of Sciences of the United States of America·Du-Chu WuSerge Przedborski
Oct 15, 2003·Neuron·Junying YuanAlexei Degterev
Feb 11, 2004·The Journal of Biological Chemistry·Susana Castro-ObregónDale E Bredesen
Feb 20, 2004·Biochemistry. Biokhimii︠a︡·N F SchorK D Nylander
Mar 20, 2004·Nature Reviews. Drug Discovery·Kevin J BarnhamAshley I Bush
May 4, 2004·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·Baochun ZhangBrian G Harbrecht

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Citations

Jan 4, 2012·Journal of Neural Transmission·Mahesh Ramalingam, Sung-Jin Kim
Jan 10, 2012·Cell Biology and Toxicology·Colette T DooleyJane H Thompson
Oct 17, 2008·The Journal of Biological Chemistry·Xuebo LiuToshihiko Osawa
Jul 4, 2012·The Journal of Clinical Investigation·Yosif M GanatLorenz Studer
Nov 13, 2013·International Journal of Molecular Sciences·Ruben K DagdaElzbieta Janda
Aug 18, 2010·The Journal of Cell Biology·Salvatore J CherraCharleen T Chu
May 1, 2009·Expert Opinion on Drug Discovery·David R Brown
Jun 15, 2006·Journal of Neuropathology and Experimental Neurology·Charleen T Chu
Nov 4, 2010·Journal of Neurochemistry·Kensuke SakamotoKarl Obrietan
Jul 23, 2013·Journal of Biochemical and Molecular Toxicology·Zeinab H MilaniRichard B Parsons
Mar 8, 2014·Cell Biology International·Yuka NishimuraNobuyuki Fukushima
Apr 10, 2015·Journal of Alzheimer's Disease : JAD·Hao WuQuan-Hong Ma
Aug 21, 2012·Biochimica Et Biophysica Acta·Vivek P PatelCharleen T Chu
Jul 15, 2009·Biochimica Et Biophysica Acta·Charleen T Chu
Dec 30, 2014·The International Journal of Biochemistry & Cell Biology·K M LawrenceP A Townsend
Dec 7, 2011·Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association·Sehwan ShimJungkee Kwon
Apr 11, 2014·Neurobiology of Disease·Jose A Santiago, Judith A Potashkin
Jan 8, 2017·Molecular Neurobiology·Dominic Ngima Nthenge-Ngumbau, Kochupurackal P Mohanakumar
Mar 30, 2018·Nutritional Neuroscience·Juen-Haur HwangYin-Ching Chan

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