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Licensed Unlicensed Requires Authentication Published by De Gruyter December 28, 2016

Redox-sensitive GFP to monitor oxidative stress in neurodegenerative diseases

  • Sonia Esposito , Alessandra Masala , Simona Sanna , Mauro Rassu , Viengsavanh Pimxayvong , Ciro Iaccarino and Claudia Crosio EMAIL logo

Abstract

Redox processes are key events in the degenerative cascade of many adult-onset neurodegenerative diseases (NDs), but the biological relevance of a single redox change is often dependent on the redox couple involved and on its subcellular origin. The biosensors based on engineered fluorescent proteins (redox-sensitive GFP [roGFP]) offer a unique opportunity to monitor redox changes in both physiological and pathological contexts in living animals and plants. Here, we review the use of roGFPs to monitor oxidative stress in different three adult-onset NDs: Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). Despite the many differences spanning from incidence to onset, the hypotheses on biological processes underlying both sporadic and familiar ND forms in humans outline a model in which noncompeting mechanisms are likely to converge in various unsuccessful patterns to mediate the selective degeneration of a specific neuronal population. roGFPs, targeted to different cell compartments, are successfully used as specific markers of cell toxicity, induced by expression of causative genes linked to a determined ND. We also report the use of roGFP to monitor oxidative stress induced by the expression of the ALS-causative gene SOD1.

Acknowledgments

This study was supported by AriSLA (pilot grant project ALSHDAC1), Regione Sardegna (grant CRP17171), and PRIN 2015 (grant 2015LFPNMN_005). We would like to acknowledge all the people from the laboratory that critically read the manuscript. Thanks are due to Manuela Galioto for technical assistance and to Giustina Casu for proofreading the manuscript for English language.

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Received: 2016-7-11
Accepted: 2016-10-2
Published Online: 2016-12-28
Published in Print: 2017-2-1

©2017 Walter de Gruyter GmbH, Berlin/Boston

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