DocumentCode
3321095
Title
Notice of Retraction
Construction of a Cellular Model for Mitochondrial Dysfunction in Alzheimer´s Disease by over Expressing Cyclophilin D
Author
Xiao Cong ; Youzheng Wang ; Wensheng Zhang
Author_Institution
Center for Natural Med. Eng., Beijing Normal Univ., Beijing, China
fYear
2011
fDate
10-12 May 2011
Firstpage
1
Lastpage
4
Abstract
Notice of Retraction
After careful and considered review of the content of this paper by a duly constituted expert committee, this paper has been found to be in violation of IEEE´s Publication Principles.
We hereby retract the content of this paper. Reasonable effort should be made to remove all past references to this paper.
The presenting author of this paper has the option to appeal this decision by contacting TPII@ieee.org.
Objective- Establish a cellular model for studying the Aβ-mediated mitochondrial dysfunction and neuronal stress in Alzheimer´s disease. Methods- The full length cDNA fragment of cyclophilin D (CCDS7358.1) was composed after codon optimization, then amplified by PCR and ligated into pcDNA3.1(+)-myc-his vector to construct the recombinant plasmid pcDNA3.1-myc-his-CypD. The SH-SY5Y neuroblastoma cells were transfected with pcDNA3.1-myc-his-CypD using lipofectamine2000 reagent, and stable transfectants were selected in 10000μg/mL G418. Transfection efficiency was examined with western bolt. Results- The sequencing analysis confirmed the accuracy of the eukaryotic expression vector pcDNA3.1-myc-his-CypD. There is no obvious effect of CypD overexpression on cell morphology, but the cell growth rate reduced. Conclusion- The establishment of stable SH-SY5Y CypD cell line provided a cellular model for mitochondrial related pathophysiology and therapy research in Alzheimer´s disease.
After careful and considered review of the content of this paper by a duly constituted expert committee, this paper has been found to be in violation of IEEE´s Publication Principles.
We hereby retract the content of this paper. Reasonable effort should be made to remove all past references to this paper.
The presenting author of this paper has the option to appeal this decision by contacting TPII@ieee.org.
Objective- Establish a cellular model for studying the Aβ-mediated mitochondrial dysfunction and neuronal stress in Alzheimer´s disease. Methods- The full length cDNA fragment of cyclophilin D (CCDS7358.1) was composed after codon optimization, then amplified by PCR and ligated into pcDNA3.1(+)-myc-his vector to construct the recombinant plasmid pcDNA3.1-myc-his-CypD. The SH-SY5Y neuroblastoma cells were transfected with pcDNA3.1-myc-his-CypD using lipofectamine2000 reagent, and stable transfectants were selected in 10000μg/mL G418. Transfection efficiency was examined with western bolt. Results- The sequencing analysis confirmed the accuracy of the eukaryotic expression vector pcDNA3.1-myc-his-CypD. There is no obvious effect of CypD overexpression on cell morphology, but the cell growth rate reduced. Conclusion- The establishment of stable SH-SY5Y CypD cell line provided a cellular model for mitochondrial related pathophysiology and therapy research in Alzheimer´s disease.
Keywords
DNA; bioinformatics; cellular biophysics; diseases; molecular biophysics; molecular configurations; neurophysiology; proteins; Aβ-mediated mitochondrial dysfunction; Alzheimer disease; PCR; SH-SY5Y neuroblastoma cells; cDNA fragment; cell growth rate; cell morphology; cellular model; codon optimization; cyclophilin D overexpression; lipofectamine2000 reagent; neuronal stress; pathophysiology; recombinant plasmid pcDNA3.1-myc-his-CypD; sequencing analysis; therapy research; transfection efficiency; Alzheimer´s disease; Calcium; Cells (biology); Cloning; Mice; Morphology; Permeability;
fLanguage
English
Publisher
ieee
Conference_Titel
Bioinformatics and Biomedical Engineering, (iCBBE) 2011 5th International Conference on
Conference_Location
Wuhan
ISSN
2151-7614
Print_ISBN
978-1-4244-5088-6
Type
conf
DOI
10.1109/icbbe.2011.5780226
Filename
5780226
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