NDLI: Transient expressions of doppel and its structural analog prionΔ32-121 in SH-SY5Y cells caused cytotoxicity possibly by triggering similar apoptosis pathway

Content Provider	Springer Nature Link
Author	Xu, K. Wang, X. Tian, C. Shi, S. Wang, G. R. Shi, Q. Li, P. Zhou, R. M. Jiang, H. Y. Chu, Y. L. Dong, X. P.
Copyright Year	2009
Abstract	Doppel (Dpl) is a recently identified prion (PrP)-like protein due to the structural and biochemical similarities, however, its natural function and pathogenic role in neurodegenerative diseases remains unclear. To investigate the possible pathogenic pathway of Dpl and its structural analog for cell apoptosis, mammalian expressing recombinant plasmids containing human PRND gene encoding the full-length Dpl and a truncated human PRNP gene deleting the sequences encoding the peptide from aa 32 to 121 (PrPΔ32-121) were generated. MTT assays showed the cell viabilities of the human neuroblastoma cell line SH-SY5Y receiving Dpl and PrPΔ32-121 expressing plasmids were remarkably lower. Obvious apoptosis phenomena were observed to be associated with the cells transient expressing Dpl and PrPΔ32-121, including reduced mitochondrial transmembrane potential (ψm), decreased pro-caspase-3 quantity, more numbers of annexin V- and annexin V/PI-double-stained cells and depressed Bcl-2 level. Moreover, we also found that the Dpl- and PrPΔ32-121-induced cytotoxicities and relevant apoptotic events in SH-SY5Y cells could be fully antagonized by co-expression of the human full-length PrP. These data highly indicate that cytotoxicity induced by the expression of Dpl and truncated PrP in neural derived cells are closely related with the apoptosis process, probably triggering the mitochondrial pathway. It also implies that the cell-benefit activity of the full-length PrP may result from its anti-apoptosis capacity.
Starting Page	2549
Ending Page	2558
Page Count	10
File Format	PDF
ISSN	03014851
Journal	Molecular Biology Reports
Volume Number	37
Issue Number	5
e-ISSN	15734978
Language	English
Publisher	Springer Netherlands
Publisher Date	2009-08-29
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Dpl PrPΔ32-121 Cytotoxicity Apoptosis Mitochondria Animal Biochemistry Animal Anatomy / Morphology / Histology
Content Type	Text
Resource Type	Article
Subject	Genetics Medicine Molecular Biology

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