Near-infrared 808 nm light boosts complex IV-dependent respiration and rescues a Parkinson-related pink1 model

Melissa Vos; Blaise Lovisa; Ann Geens; Vanessa A Morais; Georges Wagnières; Hubert van den Bergh; Alec Ginggen; Bart De Strooper; Yanik Tardy; Patrik Verstreken

doi:10.1371/journal.pone.0078562

Near-infrared 808 nm light boosts complex IV-dependent respiration and rescues a Parkinson-related pink1 model

PLoS One. 2013 Nov 11;8(11):e78562. doi: 10.1371/journal.pone.0078562. eCollection 2013.

Authors

Melissa Vos¹, Blaise Lovisa, Ann Geens, Vanessa A Morais, Georges Wagnières, Hubert van den Bergh, Alec Ginggen, Bart De Strooper, Yanik Tardy, Patrik Verstreken

Affiliation

¹ VIB Center for the Biology of Disease, Leuven, Belgium ; KU Leuven, Department of Human Genetics and Leuven Research Institute for Neuroscience and Disease (LIND), Leuven, Belgium.

Abstract

Mitochondrial electron transport chain (ETC) defects are observed in Parkinson's disease (PD) patients and in PD fly- and mouse-models; however it remains to be tested if acute improvement of ETC function alleviates PD-relevant defects. We tested the hypothesis that 808 nm infrared light that effectively penetrates tissues rescues pink1 mutants. We show that irradiating isolated fly or mouse mitochondria with 808 nm light that is absorbed by ETC-Complex IV acutely improves Complex IV-dependent oxygen consumption and ATP production, a feature that is wavelength-specific. Irradiating Drosophila pink1 mutants using a single dose of 808 nm light results in a rescue of major systemic and mitochondrial defects. Time-course experiments indicate mitochondrial membrane potential defects are rescued prior to mitochondrial morphological defects, also in dopaminergic neurons, suggesting mitochondrial functional defects precede mitochondrial swelling. Thus, our data indicate that improvement of mitochondrial function using infrared light stimulation is a viable strategy to alleviate pink1-related defects.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Adenosine Triphosphate / genetics
Adenosine Triphosphate / metabolism*
Animals
Disease Models, Animal
Drosophila Proteins / genetics
Drosophila Proteins / metabolism*
Drosophila melanogaster
Electron Transport Complex IV / genetics
Electron Transport Complex IV / metabolism*
Humans
Light
Mice
Oxygen Consumption*
Parkinson Disease / genetics
Parkinson Disease / metabolism*
Protein Serine-Threonine Kinases / genetics
Protein Serine-Threonine Kinases / metabolism*

Substances

Drosophila Proteins
Adenosine Triphosphate
Electron Transport Complex IV
PINK1 protein, Drosophila
Protein Serine-Threonine Kinases

Grants and funding

Support was provided by IWT (O&O), research fund KU Leuven, ERC StG (260678), FWO grants, Methusalem grant, the CTI (14660.1 PFLS-LS and 13758.1 PFFLE-ES), the R’EQUIP program (206021_128677), the J. Jacobi Trust, the Swiss National Science Foundation (205320 147141/1), the Hercules and Francqui Foundations, an IUAP of BELSPO and VIB as well as a fellowships from IWT, Research fund KU Leuven (PDM) and FWO to MV. The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.