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. 2020 Sep 10;8:574223. doi: 10.3389/fcell.2020.574223

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Copyright © 2020 Xiong, Zhang, Hu, Zhao, Lv, Yi, Wu and Wu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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ASC-exos function in the bone remodeling cycle. (A) In bone resorption and reversal, ASC-exos could decrease the expression of RANKL, which was highly expressed by osteoclasts or their precursors for osteoclast activation, to antagonize osteocyte-mediated osteoclastogenesis. (B) In bone formation, ASC-exos possessed the ability of lowering the production of IL-6 and PGE2, downregulating SA-β-gal activity and reducing the accumulation of γH2AX in osteoblasts. Additionally, ASC-exos could upregulate the radio of Bcl-2/Bax, diminish the production of ROS and cytochrome c, and subsequent activation of caspase-3/9 in osteocytes. ASCs, Adipose-derived stem cells; ASC-exos, ASC-derived exosomes; RANKL, Receptor Activator of Nuclear Factor Kappa B Ligand; IL-6, Interleukin 6; PGE2, Prostaglandin E2; SA-β-gal, Senescence-Associated β-galactosidase; γH2AX, Phosphorylated Histone H2AX; Bcl-2, B-cell lymphoma/leukemia 2; Bax, Bcl-2-associated X protein; Caspase-3/9, Aspartate Proteolytic Enzyme 3/9.