Autophagy machinery in the context of mammalian mitophagy

Yoshii, Saori R.; Mizushima, Noboru

doi:10.1016/j.bbamcr.2015.01.013

Cited by 83 publications

(62 citation statements)

References 70 publications

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“…It may be an attempt to eliminate damaged organelles, particularly the damaged mitochondria. Indeed damaged mitochondria are classically eliminated via mitophagy, which is a specialized type of autophagy [42]. It may also be a way to sequester and discard NPs accumulated in the cytoplasm, which is supported by our TEM observations showing cells containing numerous autolysosomes filled with NPs.…”

Section: Accepted Manuscriptsupporting

confidence: 52%

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Molecular responses of alveolar epithelial A549 cells to chronic exposure to titanium dioxide nanoparticles: A proteomic view

Armand

Biola-Clier

Bobyk

et al. 2016

Journal of Proteomics

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Our results make possible the identification of new mechanisms that explain TiO2-NP toxicity upon long-term, in vitro exposure of A549 cells. It is the first article describing -omics results obtained with this experimental strategy. We show that this long-term exposure modifies the cellular content of proteins involved in functions including mitochondrial activity, intra- and extracellular trafficking, proteasome activity, glucose metabolism, and gene expression. Moreover we observe modification of content of proteins that activate the p53 pathway, which suggest the induction of a DNA damage response. Technically, our results show that exposure of A549 cells to a high concentration of TiO2-NPs leads to the identification of modulations of the same functional categories than exposure to low, more realistic concentrations. Still the intensity differs between these two exposure scenarios. We also show that chronic exposure to TiO2-NPs induces the modulation of cellular functions that have already been reported in the literature as being impacted in acute exposure scenarios. This proves that the exposure protocol in in vitro experiments related to nanoparticle toxicology might be cautiously chosen since inappropriate scenario may lead to inappropriate and/or incomplete conclusions.

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Section: Accepted Manuscriptsupporting

confidence: 52%

“…Classically, defective mitochondria are selectively removed from cells via mitophagy, which is a specific type of autophagy, in order to prevent cell degeneration [42]. The presence of mitochondria with altered functions in cells chronically exposed to TiO 2 -NPs suggests that autophagy might be defective.…”

Section: Mitochondrial Activitymentioning

confidence: 99%

Molecular responses of alveolar epithelial A549 cells to chronic exposure to titanium dioxide nanoparticles: A proteomic view

Armand

Biola-Clier

Bobyk

et al. 2016

Journal of Proteomics

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“…Accumulated evidence suggested an interlink between autophagy and mitochondrial proteins turnover (35,51). Herein, we observed that prolonged BPA exposure impairs autophagy and enhances oxidative stress and apoptosis in the hippocampus region of the rat brain.…”

Section: Discussionmentioning

confidence: 72%

Dynamin-related Protein 1 Inhibition Mitigates Bisphenol A-mediated Alterations in Mitochondrial Dynamics and Neural Stem Cell Proliferation and Differentiation

Agarwal

Yadav

Tiwari

et al. 2016

Journal of Biological Chemistry

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The regulatory dynamics of mitochondria comprises well orchestrated distribution and mitochondrial turnover to maintain the mitochondrial circuitry and homeostasis inside the cells. Several pieces of evidence suggested impaired mitochondrial dynamics and its association with the pathogenesis of neurodegenerative disorders. We found that chronic exposure of synthetic xenoestrogen bisphenol A (BPA), a component of consumer plastic products, impaired autophagy-mediated mitochondrial turnover, leading to increased oxidative stress, mitochondrial fragmentation, and apoptosis in hippocampal neural stem cells (NSCs). It also inhibited hippocampal derived NSC proliferation and differentiation, as evident by the decreased number of BrdU-and ␤-III tubulin-positive cells. All these effects were reversed by the inhibition of oxidative stress using N-acetyl cysteine. BPA up-regulated the levels of Drp-1 (dynamin-related protein 1) and enhanced its mitochondrial translocation, with no effect on Fis-1, Mfn-1, Mfn-2, and Opa-1 in vitro and in the hippocampus. Moreover, transmission electron microscopy studies suggested increased mitochondrial fission and accumulation of fragmented mitochondria and decreased elongated mitochondria in the hippocampus of the rat brain. Impaired mitochondrial dynamics by BPA resulted in increased reactive oxygen species and malondialdehyde levels, disruption of mitochondrial membrane potential, and ATP decline. Pharmacological (Mdivi-1) and genetic (Drp-1siRNA) inhibition of Drp-1 reversed BPA-induced mitochondrial dysfunctions, fragmentation, and apoptosis. Interestingly, BPAmediated inhibitory effects on NSC proliferation and neuronal differentiations were also mitigated by Drp-1 inhibition. On the other hand, Drp-1 inhibition blocked BPA-mediated Drp-1 translocation, leading to decreased apoptosis of NSC. Overall, our studies implicate Drp-1 as a potential therapeutic target against BPA-mediated impaired mitochondrial dynamics and neurodegeneration in the hippocampus.

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“…These mitophagy pathways have been extensively reviewed. [5][6][7][8] Mitophagy is balanced by mitochondrial biogenesis for generation of new mitochondria. 9,10 Removal of damaged mitochondria via mitophagy is essential for prevention of cellular dysfunction and death.…”

Section: Introductionmentioning

confidence: 99%

New methods for monitoring mitochondrial biogenesis and mitophagy in vitro and in vivo

Williams

Zhao

Jin

et al. 2017

Exp Biol Med (Maywood)

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Removal of damaged mitochondria through mitophagy is critical for maintaining cellular homeostasis and functions. However, reliable quantitative assays to monitor mitophagy, particularly in vivo, are just emerging. This review will summarize the current novel quantitative assays to monitor mitophagy in vivo. AbstractRemoval of damaged mitochondria through mitophagy is critical for maintaining cellular homeostasis and functions. Increasing evidence implicates mitophagy in red blood cell differentiation, neurodegeneration, macrophage-mediated inflammation, ischemia, adipogenesis, drug-induced tissue injury, and cancer. Considerable progress has been made toward understanding the biochemical mechanisms involved in mitophagy regulation. However, few reliable assays to monitor and quantify mitophagy have been developed, particularly in vivo. In this review, we summarize the recent development of three assays, MitoTimer, mt-Keima and mito-QC, for monitoring and quantifying mitophagy in cells and in animal tissues. We also discuss the advantages and limitations of these three assays when using them to monitor and quantify mitophagy.

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Autophagy machinery in the context of mammalian mitophagy

Cited by 83 publications

References 70 publications

Molecular responses of alveolar epithelial A549 cells to chronic exposure to titanium dioxide nanoparticles: A proteomic view

Molecular responses of alveolar epithelial A549 cells to chronic exposure to titanium dioxide nanoparticles: A proteomic view

Dynamin-related Protein 1 Inhibition Mitigates Bisphenol A-mediated Alterations in Mitochondrial Dynamics and Neural Stem Cell Proliferation and Differentiation

New methods for monitoring mitochondrial biogenesis and mitophagy in vitro and in vivo

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