Exosomal vimentin from adipocyte progenitors protects fibroblasts against osmotic stress and inhibits apoptosis to enhance wound healing

Sepideh Parvanian; Hualian Zha; Dandan Su; Lifang Xi; Yaming Jiu; Hongbo Chen; John E. Eriksson; Fang Cheng

doi:10.3390/ijms22094678

Exosomal vimentin from adipocyte progenitors protects fibroblasts against osmotic stress and inhibits apoptosis to enhance wound healing

Sepideh Parvanian
, Hualian Zha
, Dandan Su
, Lifang Xi
, Yaming Jiu
, Hongbo Chen
, John E. Eriksson
, Fang Cheng^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › Scientific › peer-review

28 Citations (Scopus)

166 Downloads (Pure)

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.

Original language	English
Article number	4678
Journal	International Journal of Molecular Sciences
Volume	22
Issue number	9
DOIs	https://doi.org/10.3390/ijms22094678
Publication status	Published - 1 May 2021
MoE publication type	A1 Journal article-refereed

Funding

This project funded by Sigrid Juselius Stiftelse and ?bo Akademi University, the National Natural Science Foundation of China (81702750, 81670141, 81970145, 81502663, 31970660); Science, Technology & Innovation Commission of Shenzhen Municipality (JCY20170818164756460, JCYJ20180307154700308, JCYJ20170818163844015); The Social Development Foundation of Jiangsu Province (BE2018691); Natural Science Foundation of Shanghai (19ZR1463000); ?100 talents program? from the Chinese Academy of Sciences and Shanghai Talent Development Funding. Imaging studies have been done at Turku Cell Imaging. Vim?/?APCs were obtained from Genome Editing Core, Turku Bioscience Centre. TEM imaging and NTA analysis were performed by the EV Core and Electron Microscopy Unit of the Institute of Biotechnology, University of Helsinki. Funding: This project funded by Sigrid Juselius Stiftelse and Åbo Akademi University, the National Natural Science Foundation of China (81702750, 81670141, 81970145, 81502663, 31970660); Science, Technology & Innovation Commission of Shenzhen Municipality (JCY20170818164756460, JCYJ20180307154700308, JCYJ20170818163844015); The Social Development Foundation of Jiangsu Province (BE2018691); Natural Science Foundation of Shanghai (19ZR1463000); “100 talents program” from the Chinese Academy of Sciences and Shanghai Talent Development Funding. Imaging studies have been done at Turku Cell Imaging.

Keywords

Exosome
Mechanical stress
Osmotic stress
Vimentin
Wound healing

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10.3390/ijms22094678

ijms-22-04678Final published version, 4.78 MBLicence: CC BY

https://urn.fi/URN:NBN:fi-fe2022021418860

Cite this

@article{d03a80fcb3424bcd8e6e1cefc343918e,

title = "Exosomal vimentin from adipocyte progenitors protects fibroblasts against osmotic stress and inhibits apoptosis to enhance wound healing",

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{\textquoteright} 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.",

keywords = "Exosome, Mechanical stress, Osmotic stress, Vimentin, Wound healing",

author = "Sepideh Parvanian and Hualian Zha and Dandan Su and Lifang Xi and Yaming Jiu and Hongbo Chen and Eriksson, \{John E.\} and Fang Cheng",

note = "Funding Information: This project funded by Sigrid Juselius Stiftelse and ?bo Akademi University, the National Natural Science Foundation of China (81702750, 81670141, 81970145, 81502663, 31970660); Science, Technology \& Innovation Commission of Shenzhen Municipality (JCY20170818164756460, JCYJ20180307154700308, JCYJ20170818163844015); The Social Development Foundation of Jiangsu Province (BE2018691); Natural Science Foundation of Shanghai (19ZR1463000); ?100 talents program? from the Chinese Academy of Sciences and Shanghai Talent Development Funding. Imaging studies have been done at Turku Cell Imaging. Vim?/?APCs were obtained from Genome Editing Core, Turku Bioscience Centre. TEM imaging and NTA analysis were performed by the EV Core and Electron Microscopy Unit of the Institute of Biotechnology, University of Helsinki. Funding Information: Funding: This project funded by Sigrid Juselius Stiftelse and {\AA}bo Akademi University, the National Natural Science Foundation of China (81702750, 81670141, 81970145, 81502663, 31970660); Science, Technology \& Innovation Commission of Shenzhen Municipality (JCY20170818164756460, JCYJ20180307154700308, JCYJ20170818163844015); The Social Development Foundation of Jiangsu Province (BE2018691); Natural Science Foundation of Shanghai (19ZR1463000); “100 talents program” from the Chinese Academy of Sciences and Shanghai Talent Development Funding. Imaging studies have been done at Turku Cell Imaging. Publisher Copyright: {\textcopyright} 2021 by the authors. Licensee MDPI, Basel, Switzerland.",

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doi = "10.3390/ijms22094678",

language = "English",

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AU - Parvanian, Sepideh

AU - Zha, Hualian

AU - Su, Dandan

AU - Xi, Lifang

AU - Jiu, Yaming

AU - Chen, Hongbo

AU - Eriksson, John E.

AU - Cheng, Fang

N1 - Funding Information: This project funded by Sigrid Juselius Stiftelse and ?bo Akademi University, the National Natural Science Foundation of China (81702750, 81670141, 81970145, 81502663, 31970660); Science, Technology & Innovation Commission of Shenzhen Municipality (JCY20170818164756460, JCYJ20180307154700308, JCYJ20170818163844015); The Social Development Foundation of Jiangsu Province (BE2018691); Natural Science Foundation of Shanghai (19ZR1463000); ?100 talents program? from the Chinese Academy of Sciences and Shanghai Talent Development Funding. Imaging studies have been done at Turku Cell Imaging. Vim?/?APCs were obtained from Genome Editing Core, Turku Bioscience Centre. TEM imaging and NTA analysis were performed by the EV Core and Electron Microscopy Unit of the Institute of Biotechnology, University of Helsinki. Funding Information: Funding: This project funded by Sigrid Juselius Stiftelse and Åbo Akademi University, the National Natural Science Foundation of China (81702750, 81670141, 81970145, 81502663, 31970660); Science, Technology & Innovation Commission of Shenzhen Municipality (JCY20170818164756460, JCYJ20180307154700308, JCYJ20170818163844015); The Social Development Foundation of Jiangsu Province (BE2018691); Natural Science Foundation of Shanghai (19ZR1463000); “100 talents program” from the Chinese Academy of Sciences and Shanghai Talent Development Funding. Imaging studies have been done at Turku Cell Imaging. Publisher Copyright: © 2021 by the authors. Licensee MDPI, Basel, Switzerland.

PY - 2021/5/1

Y1 - 2021/5/1

N2 - 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.

AB - 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.

KW - Exosome

KW - Mechanical stress

KW - Osmotic stress

KW - Vimentin

KW - Wound healing

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DO - 10.3390/ijms22094678

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C2 - 33925176

AN - SCOPUS:85104825282

SN - 1661-6596

VL - 22

JO - International Journal of Molecular Sciences

JF - International Journal of Molecular Sciences

IS - 9

M1 - 4678

ER -

Exosomal vimentin from adipocyte progenitors protects fibroblasts against osmotic stress and inhibits apoptosis to enhance wound healing

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