Intracellular partitioning of cell organelles and extraneous nanoparticles during mitosis

Symens, Nathalie; Soenen, Stefaan J.; Rejman, Joanna; Braeckmans, Kevin; Smedt, Stefaan C. De

doi:10.1016/j.addr.2011.11.012

Cited by 47 publications

(29 citation statements)

References 196 publications

(308 reference statements)

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“…There may also be an eventual loss of the total nanomaterial load per cell as a result of mitotic division, nanomaterial exocytosis, and/or transcytosis (for reviews see refs. ).…”

Section: Cellular Uptake and Fate Of Nanomaterialsmentioning

confidence: 97%

Biodistribution, Clearance, and Long‐Term Fate of Clinically Relevant Nanomaterials

et al. 2018

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Realization of the immense potential of nanomaterials for biomedical applications will require a thorough understanding of how they interact with cells, tissues, and organs. There is evidence that, depending on their physicochemical properties and subsequent interactions, nanomaterials are indeed taken up by cells. However, the subsequent release and/or intracellular degradation of the materials, transfer to other cells, and/or translocation across tissue barriers are still poorly understood. The involvement of these cellular clearance mechanisms strongly influences the long-term fate of used nanomaterials, especially if one also considers repeated exposure. Several nanomaterials, such as liposomes and iron oxide, gold, or silica nanoparticles, are already approved by the American Food and Drug Administration for clinical trials; however, there is still a huge gap of knowledge concerning their fate in the body. Herein, clinically relevant nanomaterials, their possible modes of exposure, as well as the biological barriers they must overcome to be effective are reviewed. Furthermore, the biodistribution and kinetics of nanomaterials and their modes of clearance are discussed, knowledge of the long-term fates of a selection of nanomaterials is summarized, and the critical points that must be considered for future research are addressed.

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“…There may also be an eventual loss of the total nanomaterial load per cell as a result of mitotic division, nanomaterial exocytosis, and/or transcytosis (for reviews see refs. ).…”

Section: Cellular Uptake and Fate Of Nanomaterialsmentioning

confidence: 97%

Biodistribution, Clearance, and Long‐Term Fate of Clinically Relevant Nanomaterials

et al. 2018

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“…During prophase the nuclear envelope is disassembled and the chromatids are exposed to the cytoplasm. Particles may then associate with the DNA before the nuclear envelope reassembles during telophase [107]. …”

Section: Intracellular Localizationmentioning

confidence: 99%

Odyssey of a cancer nanoparticle: From injection site to site of action

Nichols¹,

Bae²

2012

Nano Today

336

275

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No chemotherapeutic drug can be effective until it is delivered to its target site. Nano-sized drug carriers are designed to transport therapeutic or diagnostic materials from the point of administration to the drug’s site of action. This task requires the nanoparticle carrying the drug to complete a journey from the injection site to the site of action. The journey begins with the injection of the drug carrier into the bloodstream and continues through stages of circulation, extravasation, accumulation, distribution, endocytosis, endosomal escape, intracellular localization and—finally—action. Effective nanoparticle design should consider all of these stages to maximize drug delivery to the entire tumor and effectiveness of the treatment.

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“…Active segregation in metazoans is carried out through attachment to microtubules primarily, a prime example being chromosomal inheritance. For passive segregation, organelles are not associated with the cytoskeleton and a simple increase in their abundance is thought to allow for stochastic and balanced inheritance into daughter cells (Symens et al, 2012). Mitochondria are thought to undergo passive inheritance, although it is unclear how it comes about.…”

Section: Introductionmentioning

confidence: 99%

Phosphorylation-Induced Motor Shedding Is Required at Mitosis for Proper Distribution and Passive Inheritance of Mitochondria

2016

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While interphase mitochondria associate with microtubules, mitotic mitochondria dissociate from spindle microtubules and localize in the cell periphery. Here, we show that this redistribution is not mediated by mitochondrial active transport or tethering to the cytoskeleton. Instead, kinesin and dynein, that link mitochondria to microtubules, are shed from the mitochondrial surface. Shedding is driven by phosphorylation of mitochondrial and cytoplasmic targets by CDK1 and Aurora A. Forced recruitment of motor proteins to mitotic mitochondria to override this shedding prevents their proper symmetrical distribution and disrupts the balanced inheritance of mitochondria to daughter cells. Moreover, when mitochondria with bound dynein bind to the mitotic spindle, they arrest cell cycle progression and produce binucleate cells. Thus, our results show that the regulated release of motor proteins from the mitochondrial surface is a critical mitotic event.

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Intracellular partitioning of cell organelles and extraneous nanoparticles during mitosis

Cited by 47 publications

References 196 publications

Biodistribution, Clearance, and Long‐Term Fate of Clinically Relevant Nanomaterials

Biodistribution, Clearance, and Long‐Term Fate of Clinically Relevant Nanomaterials

Odyssey of a cancer nanoparticle: From injection site to site of action

Phosphorylation-Induced Motor Shedding Is Required at Mitosis for Proper Distribution and Passive Inheritance of Mitochondria

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