The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Bioenergetics of neurons inhibit the translocation response of Parkin following rapid mitochondrial depolarization
Open accessAbstract
Recent studies delineate a pathway involving familial Parkinson's disease (PD)-related proteins PINK1 and Parkin, in which PINK1-dependent mitochondrial accumulation of Parkin targets depolarized mitochondria towards degradation through mitophagy. The pathway has been primarily characterized in cells less dependent on mitochondria for energy production than neurons. Here we report that in neurons, unlike other cells, mitochondrial depolarization by carbonyl cyanide m-chlorophenyl hydrazone did not induce Parkin translocation to mitochondria or mitophagy. PINK1 overexpression increased basal Parkin accumulation on neuronal mitochondria, but did not sensitize them to depolarization-induced Parkin translocation. Our data suggest that bioenergetic differences between neurons and cultured cell lines contribute to these different responses. In HeLa cells utilizing usual glycolytic metabolism, mitochondrial depolarization robustly triggered Parkin-mitochondrial translocation, but this did not occur in HeLa cells forced into dependence on mitochondrial respiration. Declining ATP levels after mitochondrial depolarization correlated with the absence of induced Parkin-mitochondrial translocation in both HeLa cells and neurons. However, intervention allowing neurons to maintain ATP levels after mitochondrial depolarization only modestly increased Parkin recruitment to mitochondria, without evidence of increased mitophagy. These data suggest that changes in ATP levels are not the sole determinant of the different responses between neurons and other cell types, and imply that additional mechanisms regulate mitophagy in neurons. Since the Parkin-mitophagy pathway is heavily dependent on bioenergetic status, the unique metabolic properties of neurons likely influence the function of this pathway in the pathogenesis of PD.
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Citations
Cites
Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
Narendra, D., Tanaka, A., Suen, D.-F., & Youle, R. J. (2008) · The Journal of Cell Biology · doi:10.1083/jcb.200809125 · Cited by 4,026
Guidelines for the use and interpretation of assays for monitoring autophagy
Klionsky, D. J., Abdalla, F. C., Abeliovich, H., Abraham, R. T., Acevedo-Arozena, A., Adeli, K., Agholme, L., Agnello, M., Agostinis, P., Aguirre-Ghiso, J. A., et al. (2012) · Autophagy · doi:10.4161/auto.19496 · Cited by 3,996 · cited 1×
“To examine mitophagy under these conditions, cortical neurons were co-transfected to express a GFP-tagged form of LC3 (LC3-GFP), which localizes to early autophagic vesicles and is widely used as a marker of autophagy (29), along with mtDsRed2 and hu-Parkin.”
MethodSelf-citationHereditary Early-Onset Parkinson's Disease Caused by Mutations in PINK1
Valente, E. M., Abou-Sleiman, P. M., Caputo, V., Muqit, M. M. K., Harvey, K., Gispert, S., Ali, Z., Del Turco, D., Bentivoglio, A. R., Healy, D. G., et al. (2004) · Science · doi:10.1126/science.1096284 · Cited by 3,481
PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin
Narendra, D. P., Jin, S. M., Tanaka, A., Suen, D.-F., Gautier, C. A., Shen, J., Cookson, M. R., & Youle, R. J. (2010) · PLoS Biology · doi:10.1371/journal.pbio.1000298 · Cited by 2,944
PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1
Geisler, S., Holmström, K. M., Skujat, D., Fiesel, F. C., Rothfuss, O. C., Kahle, P. J., & Springer, W. (2010) · Nature Cell Biology · doi:10.1038/ncb2012 · Cited by 2,835
Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes
Klionsky, D. J., Abeliovich, H., Agostinis, P., Agrawal, D. K., Aliev, G., Askew, D. S., Baba, M., Baehrecke, E. H., Bahr, B. A., Ballabio, A., et al. (2008) · Autophagy · doi:10.4161/auto.5338 · Cited by 2,230
Self-citationPINK1-dependent recruitment of Parkin to mitochondria in mitophagy
Vives-Bauza, C., Zhou, C., Huang, Y., Cui, M., de Vries, R. L. A., Kim, J., May, J., Tocilescu, M. A., Liu, W., Ko, H. S., et al. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0911187107 · Cited by 1,616
Evidence that glutamine, not sugar, is the major energy source for cultured HeLa cells.
Reitzer, L. J., Wice, B. M., & Kennell, D. (1979) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)30124-2 · Cited by 1,240
The PINK1/Parkin pathway regulates mitochondrial morphology
Poole, A. C., Thomas, R. E., Andrews, L. A., McBride, H. M., Whitworth, A. J., & Pallanck, L. J. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0709336105 · Cited by 885
Mitophagy in Yeast Occurs through a Selective Mechanism
Kanki, T., & Klionsky, D. J. (2008) · Journal of Biological Chemistry · doi:10.1074/jbc.m802403200 · Cited by 335
Cited by
The pathways of mitophagy for quality control and clearance of mitochondria
Ashrafi, G., & Schwarz, T. L. (2013) · Cell Death & Differentiation · doi:10.1038/cdd.2012.81 · Cited by 1,900
Chu, C. T., Ji, J., Dagda, R. K., Jiang, J. F., Tyurina, Y. Y., Kapralov, A. A., Tyurin, V. A., Yanamala, N., Shrivastava, I. H., Mohammadyani, D., et al. (2013) · Nature Cell Biology · doi:10.1038/ncb2837 · Cited by 1,083
Self-citationUnderstanding Dopaminergic Cell Death Pathways in Parkinson Disease
Michel, P. P., Hirsch, E. C., & Hunot, S. (2016) · Neuron · doi:10.1016/j.neuron.2016.03.038 · Cited by 600
Loss of iron triggers PINK1/Parkin‐independent mitophagy
Allen, G. F. G., Toth, R., James, J., & Ganley, I. G. (2013) · The EMBO Reports · doi:10.1038/embor.2013.168 · Cited by 555
Ashrafi, G., Schlehe, J. S., LaVoie, M. J., & Schwarz, T. L. (2014) · Journal of Cell Biology · doi:10.1083/jcb.201401070 · Cited by 502
“The PINK1–Parkin pathway is primarily characterized in nonneuronal cells, and controversy surrounds whether it plays any role in mitochondrial quality control in neuronal processes (Van Laar et al., 2011; Wang et al., 2011; Cai et al., 2012; Grenier et al., 2013).”
BackgroundResultInfluential
Metadata
- Authors
- Van Laar, V. S., Arnold, B., Cassady, S. J., Chu, C. T., Burton, E. A., & Berman, S. B.
- Venue
- Human Molecular Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-12-07
- Volume
- 20
- Issue
- 5
- Pages
- 927-940
- ISSN
- 0964-6906 (ISSN-L)
- 1460-2083
- OpenAlex
- W2146889537
- Cited by
- 225
- References
- 10
- FWCI
- 11.46
- Type
- journal article
- Language
- en
- Open access
- green
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- Van Laar, V. S., Arnold, B., Cassady, S. J., Chu, C. T., Burton, E. A., & Berman, S. B. (2011). Bioenergetics of neurons inhibit the translocation response of Parkin following rapid mitochondrial depolarization. Human Molecular Genetics. https://doi.org/10.1093/hmg/ddq531
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