Notice of RetractionConstruction of a Cellular Model for Mitochondrial Dysfunction in Alzheimer´s Disease by over Expressing Cyclophilin D

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.