Abstract
Mechanical stress following injury regulates the quality and speed of wound healing. Improper mechanotransduction can lead to impaired wound healing and scar formation. Vimentin intermediate filaments control fibroblasts’ response to mechanical stress and lack of vimentin makes cells significantly vulnerable to environmental stress. We previously reported the involvement of exosomal vimentin in mediating wound healing. Here we performed in vitro and in vivo experiments to explore the effect of wide-type and vimentin knockout exosomes in accelerating wound healing under osmotic stress condition. Our results showed that osmotic stress increases the size and enhances the release of exosomes. Furthermore, our findings revealed that exosomal vimentin enhances wound healing by protecting fibroblasts against osmotic stress and inhibiting stress-induced apoptosis. These data suggest that exosomes could be considered either as a stress modifier to restore the osmotic balance or as a conveyer of stress to induce osmotic stress-driven conditions.
Highlights
Chronic wounds have become a significant source of major mortality and morbidity, which lead to high medical costs and poor quality of life [1]
In cellular models relevant to wound healing, we found that wild type (WT)-adipocyte progenitors (APCs) tolerate osmotic stress better than vimentin knockout (Vim−/−)APCs, and WT-APC-Exos promote osmotic stressed HDFs proliferation
In the present study, prompted by our previous findings underlying the involvement of exosomal vimentin in promoting wound healing, we explored that exosomal vimentin may have a role in cell resistance to osmotic stress and cell protection against apoptosis
Summary
Chronic wounds have become a significant source of major mortality and morbidity, which lead to high medical costs and poor quality of life [1]. Mechanical forces, such as compression, tension, shear stress, osmotic pressure, and gravity regulate the quality and speed of wound healing. Hypo-osmolarity induces cell swelling whereas hyper-osmolarity causes cell shrinkage. Such osmotic imbalances detrimentally affect water flux, cell volume, and signaling pathways involved in cell proliferation, cell migration, and apoptosis [6,7]. Kruse et al reported that local hyperglycemia (hyper-osmotic stress), as well as systemic hyperglycemia, inhibited the migration of keratinocytes and fibroblasts as well as the re-epithelialization process [8]
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