Chapter 6 Practical approaches to investigate redox regulation of heat shock protein expression and intracellular glutathione redox state. / Calabrese, Vittorio; Signorile, Anna; Cornelius, Carolin; Mancuso, Cesare; Scapagnini, Giovanni; Ventimiglia, Bernardo; Ragusa, Nicolo; Dinkova-Kostova, Albena.
Methods in Enzymology. Vol. 441 Sandiego : Academic Press, 2008. p. 83-110.Research output: Chapter in Book/Report/Conference proceeding › Other chapter contribution
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TY - CHAP
T1 - Chapter 6 Practical approaches to investigate redox regulation of heat shock protein expression and intracellular glutathione redox state
A1 - Calabrese,Vittorio
A1 - Signorile,Anna
A1 - Cornelius,Carolin
A1 - Mancuso,Cesare
A1 - Scapagnini,Giovanni
A1 - Ventimiglia,Bernardo
A1 - Ragusa,Nicolo
A1 - Dinkova-Kostova,Albena
AU - Calabrese,Vittorio
AU - Signorile,Anna
AU - Cornelius,Carolin
AU - Mancuso,Cesare
AU - Scapagnini,Giovanni
AU - Ventimiglia,Bernardo
AU - Ragusa,Nicolo
AU - Dinkova-Kostova,Albena
PB - Academic Press
CY - Sandiego
PY - 2008
Y1 - 2008
N2 - <p>The products of vitagenes such as heat shock protein 32 (Hsp32, heme oxygenase 1) and Hsp70, the family of inducible cytoprotective proteins regulated by the Keap1/Nrf2/ARE pathway, and small molecule antioxidants such as glutathione provide the cell with powerful means to counteract and survive various conditions of stress. Among these protective systems, the heat shock proteins represent a highly conserved and robust way for preservation of correct protein conformation, recovery of damaged proteins, and cell survival. Their regulation is dependent on the redox status of the cell, thus redox regulation is rapidly evolving as an important metabolic modulator of cellular functions, and is being increasingly implicated in many chronic inflammatory and degenerative diseases. Protein thiols play a key role in redox sensing, and regulation of cellular redox state is crucial mediator of multiple metabolic, signalling and transcriptional processes in the brain. Nitric oxide, and reactive nitrogen species induce the transcription of vitagenes and Keap1/Nrf2/ARE-dependent genes whose functional products protect against a wide array of subsequent challenges. Emerging interest is now focusing on exogenous small molecules that are capable of activating these systems as a novel target to minimize deleterious consequences associated with free radical-induced cell damage, such as during neurodegeneration. This chapter describes methods that can be used to assess the expression of heat shock proteins and the cellular glutathione redox status and discusses their relevance to mechanisms modulating the onset and progression of neurodegenerative diseases.</p>
AB - <p>The products of vitagenes such as heat shock protein 32 (Hsp32, heme oxygenase 1) and Hsp70, the family of inducible cytoprotective proteins regulated by the Keap1/Nrf2/ARE pathway, and small molecule antioxidants such as glutathione provide the cell with powerful means to counteract and survive various conditions of stress. Among these protective systems, the heat shock proteins represent a highly conserved and robust way for preservation of correct protein conformation, recovery of damaged proteins, and cell survival. Their regulation is dependent on the redox status of the cell, thus redox regulation is rapidly evolving as an important metabolic modulator of cellular functions, and is being increasingly implicated in many chronic inflammatory and degenerative diseases. Protein thiols play a key role in redox sensing, and regulation of cellular redox state is crucial mediator of multiple metabolic, signalling and transcriptional processes in the brain. Nitric oxide, and reactive nitrogen species induce the transcription of vitagenes and Keap1/Nrf2/ARE-dependent genes whose functional products protect against a wide array of subsequent challenges. Emerging interest is now focusing on exogenous small molecules that are capable of activating these systems as a novel target to minimize deleterious consequences associated with free radical-induced cell damage, such as during neurodegeneration. This chapter describes methods that can be used to assess the expression of heat shock proteins and the cellular glutathione redox status and discusses their relevance to mechanisms modulating the onset and progression of neurodegenerative diseases.</p>
KW - NITRIC-OXIDE SYNTHASE
KW - CELLULAR STRESS-RESPONSE
KW - KAPPA-B ACTIVATION
KW - HEME OXYGENASE-1 INDUCTION
KW - COLORECTAL-CARCINOMA CELLS
KW - VASCULAR ENDOTHELIAL-CELLS
KW - HSP70 GENE-EXPRESSION
KW - RAT GLIAL-CELLS
KW - OXIDATIVE-STRESS
KW - NEURODEGENERATIVE DISORDERS
UR - http://www.scopus.com/inward/record.url?partnerID=yv4JPVwI&eid=2-s2.0-52249099052&md5=db5a7ed5f5befec0014d7f4e810308bd
U2 - 10.1016/S0076-6879(08)01206-8
DO - 10.1016/S0076-6879(08)01206-8
M1 - Other chapter contribution
VL - 441
BT - Methods in Enzymology
T2 - Methods in Enzymology
SP - 83
EP - 110
ER -