Par-4 is a mediator of neuronal degeneration associated with the pathogenesis of Alzheimer disease

Nature Medicine

Volumn 4, Issue 8, 1998, Pages 957-962

  Guo, Qing ^a   Fu, Weiming ^a   Xie, Jun ^a   Luo, Hong ^a   Sells, Stephen F ^b   Geddes, J W ^a   Bondada, Vimala ^a   Rangnekar, Vivek M ^b   Mattson, Mark P ^a  

^a UNIVERSITY OF KENTUCKY   (United States)

^b UNIVERSITY OF KENTUCKY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

LEUCINE ZIPPER PROTEIN; PRESENILIN 1; PROSTATE APOPTOSIS RESPONSE 4 PROTEIN; UNCLASSIFIED DRUG;

ADULT; AGED; ALZHEIMER DISEASE; APOPTOSIS; ARTICLE; CONTROLLED STUDY; FEMALE; GENE MUTATION; GENE OVEREXPRESSION; GENETIC SUSCEPTIBILITY; HUMAN; HUMAN CELL; HUMAN TISSUE; IMMUNOREACTIVITY; MALE; NERVE CELL DEGENERATION; NERVE CELL NECROSIS; PATHOGENESIS; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN INDUCTION;

ALZHEIMER DISEASE; AMYLOID BETA-PROTEIN; ANIMALS; APOPTOSIS; APOPTOSIS REGULATORY PROTEINS; BRAIN; CARRIER PROTEINS; CELLS, CULTURED; EMBRYO; GENE EXPRESSION REGULATION; HIPPOCAMPUS; HUMANS; INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS; LEUCINE ZIPPERS; MALE; MEMBRANE PROTEINS; MITOCHONDRIA; MUTAGENESIS, SITE-DIRECTED; NERVE DEGENERATION; NEURONS; OLIGONUCLEOTIDES, ANTISENSE; PC12 CELLS; PEPTIDE FRAGMENTS; POINT MUTATION; POLYMERASE CHAIN REACTION; PRESENILIN-1; PROSTATIC NEOPLASMS; RATS;

EID: 0031927628     PISSN: 10788956     EISSN: None     Source Type: Journal    
DOI: 10.1038/nm0898-957     Document Type: Article

References (27)

1. Sells, S. F. et al. Commonality of the gene programs induced by effectors of apoptosis in androgen-dependent and -independent prostate cells. Cell Growth Differ. 5, 457-466 (1994).
2. Sells, S. F. et al. Expression and function of the leucine zipper protein Par-4 in apoptosis. Mol. Cell. Biol. 17, 3823-3832 (1997).
3. Boghaert, E. R. et al. Immunohistochemical analysis of the proapoptotic protein Par-4 in normal rat tissues. Cell Growth Differ. 8, 881-890 (1997).
4. Mattson, M. P. Cellular actions of β-amyloid precursor protein, and its soluble and fibrillogenic peptide derivatives. Physiol. Rev. 77, 1081-1132 (1997).
5. Benzi, G. & Moretti, A. Contribution of mitochondrial alterations to brain aging. Adv. Cell Aging Gerontol. 2, 129-160 (1997).
6. Mattson, M. P. & Lindvall, O. Neurotrophic factor and cytokine signaling in the aging brain. Adv. Cell Aging Gerontol. 2, 299-345 (1997).
7. Su, J.H. et al. Immunocytochemical evidence for apoptosis in Alzheimer's disease. Neuroreport 5, 2529-2533 (1994).
8. Smale, G., Nichols, N.R. & Brady, D.R. Evidence for apoptotic cell death in Alzheimer's disease, Exp. Neurol. 133, 225-230 (1995).
9. Loo, D.T. et al. Apoptosis is induced by β amyloid in cultured central nervous system neurons. Proc. Natl. Acad. Sci. USA 90, 7951-7955 (1993).
10. Kruman, I. et al. Evidence that 4-hydroxynonenal mediates oxidative stress-induced neuronal apoptosis. J. Neurosci. 17, 5089-5100 (1997).
11. Steller, H. Mechanisms and genes of cellular suicide. Science 267, 1445-1449 (1995).
12. Kruman, I. et al. Calcium and reactive oxygen species mediate staurosporine-induced mitochondrial dysfunction and apoptosis in PC12 cells. J. Neurosci. Res. 51, 293-308 (1998).
13. Diaz-Meco, M. T. et al. The product of par-4, a gene induced during apoptosis, interacts selectively with the atypical isoforms of protein kinase C. Cell 86, 777-786 (1996).
14. Cohen, G. M. Caspases: the executioners of apoptosis. Biochem. J. 326, 1-16 (1997).
15. Keller, J. N. et al. Mitochondrial MnSOD prevents neural apoptosis and reduces ischemic brain injury: suppression of oxyradical production, lipid peroxidation and mitochondrial dysfunction. J. Neurosci. 18, 687-697 (1998).
16. St. George-Hyslop. P. et al. Genetic evidence for a novel familial Alzheimer's disease locus on chromosome 14. Nature Gen. 2, 330-334 (1992).
17. Sherrington, R. et al. Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease. Nature 375, 754-760 (1995).
18. Guo, Q. et al. Alzheimer's presenilin mutation sensitizes neural cells to apoptosis induced by trophic factor withdrawal and amyloid β-peptide: involvement of calcium and oxyradicals. J. Neurosci. 17, 4212-4222 (1997).
19. Janicki, S. & Monteiro, M. J. Increased apoptosis arising from increased expression of the Alzheimer's disease-associated presenilin-2 mutation (N141I). J. Cell Biol. 139, 485-495 (1997).
20. Guo, Q., Christakos, S., Robinson, N. & Mattson, M. P. Calbindin blocks the proapoptotic actions of mutant presenilin-1: reduced oxidative stress and preserved mitochondrial function. Proc. Natl. Acad. Sci. USA 95, 3227-3232 (1998).
21. Johnstone, R. W. et al. A novel repressor, par-4, modulates transcription and growth suppression functions of the Wilms' tumor suppressor WT1. Mol. Cell. Biol. 16, 6945-6956 (1996).
22. Lucas, M. & Sanchez-Margalet, V. Protein kinase C involvement in apoptosis. Gen. Pharmacol. 26, 881-887 (1995).
23. Goedert, M. Tau protein and the neurofibrillary pathology of Alzheimer's disease. Trends Neurosci. 16, 460-465 (1993).
24. Hardy, J. Amyloid, the presenilins and Alzheimer's disease. TINS 20, 154-159 (1997).
25. Mark, R.J., Blanc, E.M. & Mattson, M.P. Amyloid beta-peptide and oxidative cellular injury in Alzheimer's disease. Mol. Neurobiol. 12, 211-224 (1996).
26. Keller, J. N. et al. Increased sensitivity to mitochondrial toxin-induced apoptosis in neural cells expressing mutant presenilin-1 is linked to perturbed calcium homeostasis and enhanced oxyradical production. J. Neurosci. 18, 4439-4450 (1998).
27. Mattson, M. P., Robinson, N. & Guo, Q. Estrogens stabilize mitochondrial function and protect neural cells against the pro-apoptotic action of mutant presenilin-1. Neuroreport 8, 3817-3821 (1997).