PINK1 is necessary for long term survival and mitochondrial function in human dopaminergic neurons
Open accessAbstract
Parkinson's disease (PD) is a common age-related neurodegenerative disease and it is critical to develop models which recapitulate the pathogenic process including the effect of the ageing process. Although the pathogenesis of sporadic PD is unknown, the identification of the mendelian genetic factor PINK1 has provided new mechanistic insights. In order to investigate the role of PINK1 in Parkinson's disease, we studied PINK1 loss of function in human and primary mouse neurons. Using RNAi, we created stable PINK1 knockdown in human dopaminergic neurons differentiated from foetal ventral mesencephalon stem cells, as well as in an immortalised human neuroblastoma cell line. We sought to validate our findings in primary neurons derived from a transgenic PINK1 knockout mouse. For the first time we demonstrate an age dependent neurodegenerative phenotype in human and mouse neurons. PINK1 deficiency leads to reduced long-term viability in human neurons, which die via the mitochondrial apoptosis pathway. Human neurons lacking PINK1 demonstrate features of marked oxidative stress with widespread mitochondrial dysfunction and abnormal mitochondrial morphology. We report that PINK1 plays a neuroprotective role in the mitochondria of mammalian neurons, especially against stress such as staurosporine. In addition we provide evidence that cellular compensatory mechanisms such as mitochondrial biogenesis and upregulation of lysosomal degradation pathways occur in PINK1 deficiency. The phenotypic effects of PINK1 loss-of-function described here in mammalian neurons provides mechanistic insight into the age-related degeneration of nigral dopaminergic neurons seen in PD.
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Knocking down Pink1 in mouse neuronal cells leads to mitochondria with a swollen morphology.
“Consistent with the role of Parkin and Pink1 in Drosophila, knocking down Pink1 in mouse neuronal cells leads to mitochondria with a swollen morphology (Wood-Kaczmar et al., 2008).”
From New insights into the role of mitochondria in aging: mitochondrial dynamics and more (2010) · cites this paper as Wood-Kaczmar et al., 2008
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- Authors
- Wood-Kaczmar, A., Gandhi, S., Yao, Z., Abramov, A. S. Y., Miljan, E. A., Keen, G., Stanyer, L., Hargreaves, I., Klupsch, K., Deas, E., Downward, J., Mansfield, L., Jat, P., Taylor, J., Heales, S., Duchen, M. R., Latchman, D., Tabrizi, S. J., & Wood, N. W.
- Affiliations
- UCL Queen Square Institute of Neurology (GB)
- ReNeuron (United Kingdom) (GB)
- Eisai (United Kingdom) (GB)
- National Hospital for Neurology and Neurosurgery (GB)
- Cancer Research UK (GB)
- University College London (GB)
- Birkbeck, University of London (GB)
- Corresponding author
- Wood, Nicholas W.
- ORCID
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2008-06-18
- Volume
- 3
- Issue
- 6
- Pages
- e2455
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC2413012
- OpenAlex
- W2005764967
- Cited by
- 316
- References
- 66
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 8 · 2023: 6 · 2022: 14 · 2021: 12 · 2020: 13 · 2019: 13 · 2018: 14 · 2017: 14 · 2016: 8 · 2015: 15 · 2014: 24 · 2013: 23 · 2012: 31
- FWCI
- 24.16
- Type
- journal article
- Language
- en
- Update notices
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Liverpool John Moores University (acceptedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- UCL Discovery (University College London) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Funders
- Wellcome Trust
- Medical Research Council
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- PINK1, Parkinson's disease, dopaminergic neurons, mitochondrial dysfunction, oxidative stress, mitochondrial apoptosis, neurodegeneration, mitochondrial biogenesis, lysosomal degradation, neuroprotection, aging, staurosporine, neuroblastoma cells
- MeSH terms
- PTEN-Induced Putative Kinase, Animals, Cell Survival, Cells, Cultured, Dopamine, Electrophoresis, Polyacrylamide Gel, Humans, Microscopy, Fluorescence, Mitochondria, Neurons, Parkinson Disease, Protein Kinases, Blotting, Western, DNA, Complementary, Reverse Transcriptase Polymerase Chain Reaction, Microscopy, Electron, Transmission, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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