KMID : 0855520080210010031
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Korean Journal of Physical Anthropology 2008 Volume.21 No. 1 p.31 ~ p.40
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Protective Effect of HSP90 on Neuronal Cell Death-induced by ¥â-Amyloid Peptide
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Lee Hyun-Jung
Kim Do-Hee Lee Won-Bok Kim Kyung-Yong Chung Yoon-Hee Kim Sung-Su Kim Ok-Hyun
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Abstract
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In the present study, we determined the protective mechanism of HSP90 against neuronal cell death induced by A¥â.
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 A¥â significantly induced neuronal cell death. However, HSP90 induced by mild heat shock could attenuate neuronal apoptosis in A¥â 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 A¥â. However, HSP90 antisense oligonucleotide largely increase breakdown of mitochondrial membrane potential induced by A¥â.
These data suggest that HSP90 as chaperone protein significantly attenuates neuronal damage and protects neuroanl cells from neurotoxin such as A¥â.
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KEYWORD
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Amyloid beta, HSP90, Mitochondria, Bcl-2, Bax, Apoptosis
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