Korean J Phys Anthropol.  2008 Mar;21(1):31-40.

Protective Effect of HSP90 on Neuronal Cell Death-induced by beta-Amyloid Peptide

  • 1Department of Anatomy, College of Medicine, Chung-Ang University, Korea. whitefox@cau.ac.kr


In the present study, we determined the protective mechanism of HSP90 against neuronal cell death induced by Abeta. For the evaluation of protective role of HSP90, we used human neuroblastoma SK-N-SH cell lines, examined AlamarBlue assay, Western blot analysis and immunofluorescence assay. Incubation of SK-N-SH cells with Abeta significantly induced neuronal cell death. However, HSP90 induced by mild heat shock could attenuate neuronal apoptosis in Abeta treated condition. To identify the role of HSP90, we determined localization of HSP90 in SK-N-SH cells. Interestingly, HSP90 was increased and localized in mitochondria as treatment of mild heat shock. Also, treatment or increase of HSP90 largely elevated level of Bcl-2 expression, whereas inhibition of HSP90 with HSP90 antisense oligonucleotide significantly decreased Bcl-2 expression. In contrast to Bcl-2, Bax expression was regulated independently by HSP90. Moreover, increase of HSP90 could attenuate collapse of mitochondrial membrane potential induced by Abeta. However, HSP90 antisense oligonucleotide largely increase breakdown of mitochondrial membrane potential induced by Abeta. These data suggest that HSP90 as chaperone protein significantly attenuates neuronal damage and protects neuroanl cells from neurotoxin such as Abeta.


Amyloid beta (Abeta); HSP90; Mitochondria; Bcl-2; Bax; Apoptosis
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