Anti-osteoclastic effects of C-glucosidic ellagitannins mediated by actin perturbation

Actin subunits assemble into actin filaments whose dynamics and three-dimensional architectures are further regulated by a variety of cellular factors to establish the functional actin cytoskeleton. The C-glucosidic ellagitannin vescalagin and its simpler analogue vescalin, affect both the dynamics...

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Bibliographic Details
Published in:European journal of cell biology 2018-11, Vol.97 (8), p.533-545
Main Authors: Georgess, Dan, Spuul, Pirjo, Le Clainche, Christophe, Le Nihouannen, Damien, Fremaux, Isabelle, Dakhli, Thierry, Delannoy López, Daniela Melanie, Deffieux, Denis, Jurdic, Pierre, Quideau, Stéphane, Génot, Elisabeth
Format: Article
Language:English
Subjects:
Actin Cytoskeleton - metabolism
Actin dynamics
Actins - metabolism
Animals
Bone Resorption - pathology
Cell Adhesion - drug effects
Cell Differentiation
Cell Survival - drug effects
Cytoskeleton
Cytoskeleton - metabolism
Extracellular Matrix - metabolism
Glucosides - chemistry
Glucosides - pharmacology
Hydrolyzable Tannins - chemistry
Hydrolyzable Tannins - pharmacology
Life Sciences
Medicinal biology
Mice, Inbred C57BL
Osteoclast biology
Osteoclasts - cytology
Osteoclasts - drug effects
Osteoclasts - metabolism
Podosomes
Podosomes - metabolism
Polymerization
Polyphenol sciences
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Summary:Actin subunits assemble into actin filaments whose dynamics and three-dimensional architectures are further regulated by a variety of cellular factors to establish the functional actin cytoskeleton. The C-glucosidic ellagitannin vescalagin and its simpler analogue vescalin, affect both the dynamics and the ultrastructure of the actin cytoskeleton by directly binding to F-actin. Herein, we show that in vitro, the two compounds induce the formation of distinct F-actin networks characterized by different superstructures and dynamics. In living mature osteoclasts, highly specialized bone-degrading cells that constantly remodel their cytoskeleton, vescalagin and vescalin alter actin dynamics at podosomes and compromise the integrity of the podosome belt that forms the bone-degrading apparatus. Both compounds target the bone-resorbing activity at concentrations that preserve osteoclastic maturation and survival and with no detectable impact on the behaviour of bone-forming osteoblastic cells. This anti-osteoclastic activity of vescalagin and vescalin reveals the potential of targeting actin dynamics as a new therapeutic opportunity and, in this case, as a plausible approach for the local treatment of osteoporosis.
ISSN:0171-9335
1618-1298
DOI:10.1016/j.ejcb.2018.09.003