Transduced HSP27 protein protects neuronal cell death by enhancing FALS-associated SOD1 mutant activity

Jae Jin An; Yeom Pyo Lee; Dae Won Kim; Eun Joung Sohn; Hoon Jae Jeong; Hye Won Kang; Min Jae Shin; Mi Jin Kim; Eun Hee Ahn; Sang Ho Jang; Jung Hoon Kang; Tae Cheon Kang; Moo Ho Won; Oh Shin Kwon; Sung Woo Cho; Kil Soo Lee; Jinseu Park; Won Sik Eum; Soo Young Choi

doi:10.5483/BMBRep.2009.42.3.136

Transduced HSP27 protein protects neuronal cell death by enhancing FALS-associated SOD1 mutant activity

Jae Jin An, Yeom Pyo Lee, Dae Won Kim, Eun Joung Sohn, Hoon Jae Jeong, Hye Won Kang, Min Jae Shin, Mi Jin Kim, Eun Hee Ahn, Sang Ho Jang, Jung Hoon Kang, Tae Cheon Kang, Moo Ho Won, Oh Shin Kwon, Sung Woo Cho, Kil Soo Lee, Jinseu Park, Won Sik Eum, Soo Young Choi

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21 Scopus citations

Abstract

Familial Amyotrophic lateral sclerosis (FALS) is a progressive neurodegenetative disorder induced by mutations of the SOD1 gene. Heat shock protein 27 (HSP27) is well-defined as a stress-inducible protein, however the its role in ALS protection has not yet been established. To investigate the role HSP27 may have in SOD1 mutant-mediated apoptosis, human SOD1 or HSP27 genes were fused with a PEP-1 peptide in a bacterial expression vector to produce a genetic in-frame fusion protein, which was then transduced into cells. We found the purified PEP-1-HSP27 fusion proteins can be transduced efficiently into neuronal cells and protect against cell death by enhancing mutant SOD1 activity. Moreover, transduced PEP-1-HSP27 efficiently prevents protein aggregation produced by oxidative stress. These results suggest that transduced HSP27 fusion protein may be explored as a potential therapeutic agent for FALS patients.

Original language	English
Pages (from-to)	136-141
Number of pages	6
Journal	BMB Reports
Volume	42
Issue number	3
DOIs	https://doi.org/10.5483/BMBRep.2009.42.3.136
State	Published - Mar 2009

Keywords

Amyotrophic lateral sclerosis (ALS)
Cu,Zn-superoxide dismutase (SOD1)
Heat shock protein 27 (HSP27)
PEP-1 peptide
Protein transduction

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10.5483/BMBRep.2009.42.3.136

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An, J. J., Lee, Y. P., Kim, D. W., Sohn, E. J., Jeong, H. J., Kang, H. W., Shin, M. J., Kim, M. J., Ahn, E. H., Jang, S. H., Kang, J. H., Kang, T. C., Won, M. H., Kwon, O. S., Cho, S. W., Lee, K. S., Park, J., Eum, W. S., & Choi, S. Y. (2009). Transduced HSP27 protein protects neuronal cell death by enhancing FALS-associated SOD1 mutant activity. BMB Reports, 42(3), 136-141. https://doi.org/10.5483/BMBRep.2009.42.3.136

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title = "Transduced HSP27 protein protects neuronal cell death by enhancing FALS-associated SOD1 mutant activity",

abstract = "Familial Amyotrophic lateral sclerosis (FALS) is a progressive neurodegenetative disorder induced by mutations of the SOD1 gene. Heat shock protein 27 (HSP27) is well-defined as a stress-inducible protein, however the its role in ALS protection has not yet been established. To investigate the role HSP27 may have in SOD1 mutant-mediated apoptosis, human SOD1 or HSP27 genes were fused with a PEP-1 peptide in a bacterial expression vector to produce a genetic in-frame fusion protein, which was then transduced into cells. We found the purified PEP-1-HSP27 fusion proteins can be transduced efficiently into neuronal cells and protect against cell death by enhancing mutant SOD1 activity. Moreover, transduced PEP-1-HSP27 efficiently prevents protein aggregation produced by oxidative stress. These results suggest that transduced HSP27 fusion protein may be explored as a potential therapeutic agent for FALS patients.",

keywords = "Amyotrophic lateral sclerosis (ALS), Cu,Zn-superoxide dismutase (SOD1), Heat shock protein 27 (HSP27), PEP-1 peptide, Protein transduction",

author = "An, {Jae Jin} and Lee, {Yeom Pyo} and Kim, {Dae Won} and Sohn, {Eun Joung} and Jeong, {Hoon Jae} and Kang, {Hye Won} and Shin, {Min Jae} and Kim, {Mi Jin} and Ahn, {Eun Hee} and Jang, {Sang Ho} and Kang, {Jung Hoon} and Kang, {Tae Cheon} and Won, {Moo Ho} and Kwon, {Oh Shin} and Cho, {Sung Woo} and Lee, {Kil Soo} and Jinseu Park and Eum, {Won Sik} and Choi, {Soo Young}",

year = "2009",

month = mar,

doi = "10.5483/BMBRep.2009.42.3.136",

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An, JJ, Lee, YP, Kim, DW, Sohn, EJ, Jeong, HJ, Kang, HW, Shin, MJ, Kim, MJ, Ahn, EH, Jang, SH, Kang, JH, Kang, TC, Won, MH, Kwon, OS, Cho, SW, Lee, KS, Park, J, Eum, WS & Choi, SY 2009, 'Transduced HSP27 protein protects neuronal cell death by enhancing FALS-associated SOD1 mutant activity', BMB Reports, vol. 42, no. 3, pp. 136-141. https://doi.org/10.5483/BMBRep.2009.42.3.136

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AU - Lee, Yeom Pyo

AU - Kim, Dae Won

AU - Sohn, Eun Joung

AU - Jeong, Hoon Jae

AU - Kang, Hye Won

AU - Shin, Min Jae

AU - Kim, Mi Jin

AU - Ahn, Eun Hee

AU - Jang, Sang Ho

AU - Kang, Jung Hoon

AU - Kang, Tae Cheon

AU - Won, Moo Ho

AU - Kwon, Oh Shin

AU - Cho, Sung Woo

AU - Lee, Kil Soo

AU - Park, Jinseu

AU - Eum, Won Sik

AU - Choi, Soo Young

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N2 - Familial Amyotrophic lateral sclerosis (FALS) is a progressive neurodegenetative disorder induced by mutations of the SOD1 gene. Heat shock protein 27 (HSP27) is well-defined as a stress-inducible protein, however the its role in ALS protection has not yet been established. To investigate the role HSP27 may have in SOD1 mutant-mediated apoptosis, human SOD1 or HSP27 genes were fused with a PEP-1 peptide in a bacterial expression vector to produce a genetic in-frame fusion protein, which was then transduced into cells. We found the purified PEP-1-HSP27 fusion proteins can be transduced efficiently into neuronal cells and protect against cell death by enhancing mutant SOD1 activity. Moreover, transduced PEP-1-HSP27 efficiently prevents protein aggregation produced by oxidative stress. These results suggest that transduced HSP27 fusion protein may be explored as a potential therapeutic agent for FALS patients.

AB - Familial Amyotrophic lateral sclerosis (FALS) is a progressive neurodegenetative disorder induced by mutations of the SOD1 gene. Heat shock protein 27 (HSP27) is well-defined as a stress-inducible protein, however the its role in ALS protection has not yet been established. To investigate the role HSP27 may have in SOD1 mutant-mediated apoptosis, human SOD1 or HSP27 genes were fused with a PEP-1 peptide in a bacterial expression vector to produce a genetic in-frame fusion protein, which was then transduced into cells. We found the purified PEP-1-HSP27 fusion proteins can be transduced efficiently into neuronal cells and protect against cell death by enhancing mutant SOD1 activity. Moreover, transduced PEP-1-HSP27 efficiently prevents protein aggregation produced by oxidative stress. These results suggest that transduced HSP27 fusion protein may be explored as a potential therapeutic agent for FALS patients.

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KW - Cu,Zn-superoxide dismutase (SOD1)

KW - Heat shock protein 27 (HSP27)

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SP - 136

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JO - BMB Reports

JF - BMB Reports

IS - 3

ER -

Transduced HSP27 protein protects neuronal cell death by enhancing FALS-associated SOD1 mutant activity

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