WWW.JNEUROSCI.ORG
-
The Journal of Neuroscience
QUICK SEARCH:   [advanced]


     
-


HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP
The Journal of Neuroscience, July 2, 2003, 23(13):5789-5798

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit an eLetter
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (82)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Batulan, Z.
Right arrow Articles by Durham, H. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Batulan, Z.
Right arrow Articles by Durham, H. D.

 Previous Article  |  Next Article 

High Threshold for Induction of the Stress Response in Motor Neurons Is Associated with Failure to Activate HSF1

Zarah Batulan,1 Gayle A. Shinder,1 Sandra Minotti,1 Bei Ping He,2 Mohammad M. Doroudchi,1 Josephine Nalbantoglu,1 Michael J. Strong,2,3 and Heather D. Durham1

1Montreal Neurological Institute and Department of Neurology and Neurosurgery, McGill University, Montreal, Quebec, Canada H3A 2B4, 2Neurodegeneration Research Group, The John P. Robarts Research Institute, and 3Department of Clinical Neurological Sciences, The University of Western Ontario, London, Ontario, Canada N6A 5A5

Heat shock protein 70 (Hsp70) protects cultured motor neurons from the toxic effects of mutations in Cu/Zn-superoxide dismutase (SOD-1), which is responsible for a familial form of the disease, amyotrophic lateral sclerosis (ALS). Here, the endogenous heat shock response of motor neurons was investigated to determine whether a high threshold for activating this protective mechanism contributes to their vulnerability to stresses associated with ALS. When heat shocked, cultured motor neurons failed to express Hsp70 or transactivate a green fluorescent protein reporter gene driven by the Hsp70 promoter, although Hsp70 was induced in glial cells. No increase in Hsp70 occurred in motor neurons after exposure to excitotoxic glutamate or expression of mutant SOD-1 with a glycine-> alanine substitution at residue 93 (G93A), nor was Hsp70 increased in spinal cords of G93A SOD-1 transgenic mice or sporadic or familial ALS patients. In contrast, strong Hsp70 induction occurred in motor neurons with expression of a constitutively active form of heat shock transcription factor (HSF)-1 or when proteasome activity was sufficiently inhibited to induce accumulation of an alternative transcription factor HSF2. These results indicate that the high threshold for induction of the stress response in motor neurons stems from an impaired ability to activate the main heat shock–stress sensor, HSF1.

Key words: ALS; amyotrophic lateral sclerosis; heat shock; HSF1; HSF2; Hsp70; motor neuron; proteasome inhibition

Received Mar. 3, 2003; revised Apr. 14, 2003; accepted Apr. 21, 2003.




This article has been cited by other articles:


Home page
 Hum Mol GenetHome page
C. L. Simpson, R. Lemmens, K. Miskiewicz, W. J. Broom, V. K. Hansen, P. W.J. van Vught, J. E. Landers, P. Sapp, L. Van Den Bosch, J. Knight, et al.
Variants of the elongator protein 3 (ELP3) gene are associated with motor neuron degeneration
Hum. Mol. Genet., February 1, 2009; 18(3): 472 - 481.
[Abstract] [Full Text] [PDF]

Home page
 Genes Dev.Home page
R. I. Morimoto
Proteotoxic stress and inducible chaperone networks in neurodegenerative disease and aging
Genes & Dev., June 1, 2008; 22(11): 1427 - 1438.
[Abstract] [Full Text] [PDF]

Home page
 BrainHome page
E. V. Ilieva, V. Ayala, M. Jove, E. Dalfo, D. Cacabelos, M. Povedano, M. J. Bellmunt, I. Ferrer, R. Pamplona, and M. Portero-Otin
Oxidative and endoplasmic reticulum stress interplay in sporadic amyotrophic lateral sclerosis
Brain, December 1, 2007; 130(12): 3111 - 3123.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
D. J. Gifondorwa, M. B. Robinson, C. D. Hayes, A. R. Taylor, D. M. Prevette, R. W. Oppenheim, J. Caress, and C. E. Milligan
Exogenous Delivery of Heat Shock Protein 70 Increases Lifespan in a Mouse Model of Amyotrophic Lateral Sclerosis
J. Neurosci., November 28, 2007; 27(48): 13173 - 13180.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
D. M. Taylor, B. F. Gibbs, E. Kabashi, S. Minotti, H. D. Durham, and J. N. Agar
Tryptophan 32 Potentiates Aggregation and Cytotoxicity of a Copper/Zinc Superoxide Dismutase Mutant Associated with Familial Amyotrophic Lateral Sclerosis
J. Biol. Chem., June 1, 2007; 282(22): 16329 - 16335.
[Abstract] [Full Text] [PDF]

Home page
 ANN BOT (LOND)Home page
G. MILLER and R. MITTLER
Could Heat Shock Transcription Factors Function as Hydrogen Peroxide Sensors in Plants?
Ann. Bot., August 1, 2006; 98(2): 279 - 288.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
K. Phanvijhitsiri, M. W. Musch, M. J. Ropeleski, and E. B. Chang
Heat induction of heat shock protein 25 requires cellular glutamine in intestinal epithelial cells
Am J Physiol Cell Physiol, August 1, 2006; 291(2): C290 - C299.
[Abstract] [Full Text] [PDF]

Home page
 NeurologyHome page
B. J. Traynor, L. Bruijn, R. Conwit, F. Beal, G. O'Neill, S. C. Fagan, and M. E. Cudkowicz
Neuroprotective agents for clinical trials in ALS: A systematic assessment.
Neurology, July 11, 2006; 67(1): 20 - 27.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
H.-Y. Shen, J.-C. He, Y. Wang, Q.-Y. Huang, and J.-F. Chen
Geldanamycin Induces Heat Shock Protein 70 and Protects against MPTP-induced Dopaminergic Neurotoxicity in Mice
J. Biol. Chem., December 2, 2005; 280(48): 39962 - 39969.
[Abstract] [Full Text] [PDF]

Home page
 J Clin PharmacolHome page
R. B. Choudry and M. E. Cudkowicz
Clinical Trials in Amyotrophic Lateral Sclerosis: The Tenuous Past and the Promising Future
J. Clin. Pharmacol., December 1, 2005; 45(12): 1334 - 1344.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
J. Magrane, K. M. Rosen, R. C. Smith, K. Walsh, G. K. Gouras, and H. W. Querfurth
Intraneuronal {beta}-Amyloid Expression Downregulates the Akt Survival Pathway and Blunts the Stress Response
J. Neurosci., November 23, 2005; 25(47): 10960 - 10969.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
M. Katsuno, C. Sang, H. Adachi, M. Minamiyama, M. Waza, F. Tanaka, M. Doyu, and G. Sobue
Pharmacological induction of heat-shock proteins alleviates polyglutamine-mediated motor neuron disease
PNAS, November 15, 2005; 102(46): 16801 - 16806.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
A. Tiwari, Z. Xu, and L. J. Hayward
Aberrantly Increased Hydrophobicity Shared by Mutants of Cu,Zn-Superoxide Dismutase in Familial Amyotrophic Lateral Sclerosis
J. Biol. Chem., August 19, 2005; 280(33): 29771 - 29779.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
H. Tummala, C. Jung, A. Tiwari, C. M. J. Higgins, L. J. Hayward, and Z. Xu
Inhibition of Chaperone Activity Is a Shared Property of Several Cu,Zn-Superoxide Dismutase Mutants That Cause Amyotrophic Lateral Sclerosis
J. Biol. Chem., May 6, 2005; 280(18): 17725 - 17731.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. ProteomicsHome page
K. Fukada, F. Zhang, A. Vien, N. R. Cashman, and H. Zhu
Mitochondrial Proteomic Analysis of a Cell Line Model of Familial Amyotrophic Lateral Sclerosis
Mol. Cell. Proteomics, December 1, 2004; 3(12): 1211 - 1223.
[Abstract] [Full Text] [PDF]


-
-

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help
-
Copyright 2009 by Society for Neuroscience ONLINE ISSN: 1529-2401
-