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Aß(25-35) Peptide Induces Cell Death in PC12 Cells via Mitochondrial Damage and Cytochrome c Release



Cristiana Carelli Alinovi , Michela Pezzotti , Daniele Mezzogori , M. Elisabetta Clementi , Francesco Misiti , Bruno Giardina and Federica Orsini
 
ABSTRACT

The pathological features of Alzheimer`s disease include deposition of senile plaques in different brain zones formed by aggregates of fibrillar Aß peptide (AßP), a neurotoxic metabolic product. In this study we used the soluble form of fragment 25-35 of AßP, that includes methionine 35, side chain of AßP, to investigate the role of redox state of Met-35 on the pathogenesis of AD, because this residue in AßP is the most susceptible to oxidation in vivo. The data obtained evidenced that Aß(25-35) peptide determines a loss of PC12 cells viability determining mitochondrial damage with a possible trigger of pro-apoptotic signals. In particular, the following parameters were examined: cytochrome c release, mitochondrial membrane potential (ΔΨm) and mitochondrial respiration. In this study, three different peptides have been used: Aß(25-35) with methionine 35 in the reduced state, oxidized to sulfoxide and/or substituted with norleucine. We conclude that alteration in the mitochondrial functionality might be a contributing factor to the pathogenesis of AD and the amplitude of the effects elicited by Aß peptide is modulated by the redox state of methionine.

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  How to cite this article:

Cristiana Carelli Alinovi , Michela Pezzotti , Daniele Mezzogori , M. Elisabetta Clementi , Francesco Misiti , Bruno Giardina and Federica Orsini , 2006. Aß(25-35) Peptide Induces Cell Death in PC12 Cells via Mitochondrial Damage and Cytochrome c Release . Journal of Biological Sciences, 6: 140-145.

DOI: 10.3923/jbs.2006.140.145

URL: https://scialert.net/abstract/?doi=jbs.2006.140.145

REFERENCES
Boland, K., M. Behrens, D. Choi, K. Manias and D.H. Perlmutter, 1996. The serpin-enzyme complex receptor recognizes soluble, nontoxic amyloid-beta peptide but not aggregated, cytotoxic amyloid-beta peptide. J. Biol. Chem., 271: 18032-18044.
CrossRef  |  

Buchet, R., E. Tavitian, D. Ristig, R. Swoboda, U. Stauss and H.U. Gremlich, 1996. Conformation of synthetic β peptides in solid state and in aqueous solution relation to toxicity in PC12 cells. Biochem. Biophys. Acta, 1315: 40-46.
CrossRef  |  

Cardoso, S.M., R.H. Swerdlow and C.R. Oliveira, 2002. Induction of cytochrome c mediated apoptosis by amyloid β 25-35 requires functional mitochondria. Brain. Res., 931: 117-125.
Direct Link  |  

Casley, C.S, J.M. Land, M.A. Sharpe, J.B. Clark, M.R. Duchen and L. Canevari, 2002. β amyloid fragment 25-35 causes mitochondrial dysfunction in primary cortical neurons. Neurobiol. Dis., 10: 258-267.

Clementi, M.E., G.E. Martorana, M. Pezzotti, B. Giardina and F. Misiti, 2004. Methionine 35 oxidation reduces toxic effects of the amyloid β protein fragment (31-35) on human red blood cell. Int. J. Biochem. Cell Biol., 36: 2066-2076.
CrossRef  |  

Cory, A.H., T.C. Owen, J.A. Barltrop and J.G. Cory, 1991. Use of an aqueous soluble tetrazolium formazan assay for cell growth assays in culture. Cancer. Commun., 3: 207-212.
PubMed  |  

Dahlgren, K.N., A.M. Manelli, W.B.Jr. Stine, L.K. Baker, G.A. Krafft and M.J. LaDu, 2002. Oligomeric and fibrillar species of amyloid β peptides differentially affect neuronal viability. J. Biol. Chem., 277: 32046-32053.
Direct Link  |  

Green, D.R. and J.C. Reed, 1998. Mitochondria and apoptosis. Science, 281: 1309-1312.
CrossRef  |  PubMed  |  Direct Link  |  

Hong, J. and C. Schoneich, 2001. The metal catalyzed oxidation of methionine in peptides by fenton systems involves two consecutive one electron oxidation processes. Free Radic. Biol. Med., 31: 1342-1441.
PubMed  |  

Iuvone, T., G. Esposito, R. Esposito, R. Santamaria, M.D. Rosa and A.A. Izzo, 2004. Neuroprotective effect of cannabidiol a non psychoactive component from Cannabis sativa on β amyloid induced toxicity in PC12 cells. J. Neorochem., 89: 134-141.
Direct Link  |  

Kim, H.S., J.H. Lee, J.P. Lee, E.M. Kim and K.A. Chang et al., 2002. Amyloid β peptide induces cytochrome c release from isolated mitochondria. Neuroreport., 13: 1989-1993.
Direct Link  |  

Kuo, Y.M., T.A. Kokjohn, T.G. Beach and L.I. Sue et al., 2001. Comparative analysis of amyloid β chemical structure and amyloid plaque morphology of transgenic mouse and Alzheimer's disease brains. J. Biol. Chem., 276: 12991-12998.

Mattson, M.P., B. Cheng, D. David, K. Bryant, I. Leiberburg and R.E. Rydel, 1992. β amyloid peptides destabilize calcium homeostasis and render human cortical neurons vulnerable to excitotoxicity. J. Neuroscience, 12: 376-389.
Direct Link  |  

Meei, H.H., F. Corinne, X. Hui, Z. Hui and G.E. Gibson, 2004. Mitochondrial function in fibroblasts with aging in culture and or Alzheimers disease. Neurobiol. Aging, 26: 839-848.

Misiti, F., B. Sampaolese, M. Pezzotti, S. Marini and M.E. Clementi et al., 2005. Aβ (31-35) peptide induces apoptosis in PC12 cells contrast with Aβ (25-35) peptide and examination of underlying mechanisms. Neurochem. Int., 46: 575-583.
Direct Link  |  

Misiti, F., G.E. Martorana, G. Nocca, E. Di Stasio, B. Giardina and M.E. Clementi, 2004. Methionine 35 oxidation reduces toxic and pro-apoptotic effects af the amyloid beta-protein fragment (31-35) on isolated brain mitochondria. Neuroscience, 126: 297-303.
CrossRef  |  Direct Link  |  

Nicholls, D.G. and S.L. Budd, 2000. Mitochondria and neuronal survival. Physiol. Rev., 80: 315-360.
Direct Link  |  

Nista, E.C., M. Candelli, F. Cremonini, I.A. Cazzato and A. Gasbarrini et al., 2004. Bacillus clausii therapy to reduce side effects of anti Helicobacter pylori treatment randomized double blind placebo controlled trial. Ail. Pharmacol. Ther., 20: 1181-1188.
PubMed  |  

Pike, C.J., A.J.W. Wasserman, J. Kosmoski, D.H. Cribbs, C.G. Glabe and C.W. Cotman, 1995. Structure activity analyses of β amyloid peptides contributions of the β 25-35 region to aggregation and neurotoxicity. J. Neurochem., 64: 253-265.
Direct Link  |  

Pike, C.J., D. Burdick, A.J. Walencewicz, C.G. Glabe and C.W. Cotman, 1993. Neurodegeneration induced by β amyloid peptides In vitro the role of peptide assembly state. J. Neurosci., 13: 1676-1678.
Direct Link  |  

Preston, M.R., J.D. Estermyer, J. Kelly and P.E. Mason, 1996. Alzheimers disease amyloid β peptide 25-35 is localized in the membrane hydrocarbon core x ray diffraction analysis. Biochem. Biophys. Res. Commun., 222: 78-82.

Qiao, H., R.C. Koya, K. Nakagawa, H. Tanaka, H. Fujita, M. Takimoto and N. Kuzumaky, 2005. Inhibition of Alzheimers amyloid β peptide induced reduction of mitochondrial membrane potential and neurotoxicity by gelsolin. Neurobiol. Aging., 26: 849-855.
Direct Link  |  

Scaduto, R.C. and L.W. Grotyohann, 1999. Measurement of mitochondrial membrane potential using fluorescent rhodamine derivatives. J. Biophys., 76: 469-477.
Direct Link  |  

Smith, M.A., C.A. Rottkamp, A. Nunomura, A.K. Raina and G. Perry, 2000. Oxidative stress in Alzheimer's disease. Biochimica Biophysica Acta (BBA)-Mol. Basis Dis., 1502: 139-144.
CrossRef  |  PubMed  |  Direct Link  |  

Varadarajan, S., J. Kanski, M. Aksenova, C. Lauderback and D.A. Butterfield, 2001. Different mechanisms of oxidative stress and neurotoxicity for Alzheimer's Aβ(1--42) and Aβ(25-35). J. Am.. Chem. Soc., 123: 5625-5631.
CrossRef  |  

Varadarajan, S., S. Yatin, M. Aksenova and D.A. Butterfield, 2000. Alzheimers amyloid β peptide associated free radical oxidative stress and neurotoxicity. J. Struct. Biol., 130: 184-208.

Watson, A.A., D.P. Fairlie and D.J. Craik, 1998. Solution structure of methionine oxidized amyloid β peptide (1-40) does oxidation affect conformational switching. Biochem., 37: 12700-12706.
CrossRef  |  

Wood, S.J., B. Maleeff, T. Hart and R. Wetzel, 1996. Physical morphological and functional differences between pH 5.8 and 7.4 aggregates of the Alzheimer's amyloid peptide Aβ. J. Mol. Biol., 256: 870-877.

Xiao, X.Q., H.Y. Zhang and X.C. Tang, 2002. Huperzine a attenuates amyloid β peptide fragment 25-35 induces apoptotic in rat cortical neurons via inhibiting reactive oxigen species formation and caspase 3activation. J. Neurosi. Res., 67: 30-36.
Direct Link  |  

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