Annexin A1 released from epithelial extracellular vesicles and synthetic nanoparticles promotes wound repair

Miguel Quiros; Giovanna Leoni; Nazila Kamaly; Philipp-Alexander Neumann; Hikaru Nishio; Gabrielle Fredman; Mohammad Alam; Dennis Kusters; Chris Reutelingsperger; Mauro Perretti; Charles A. Parkos; Omid C. Farokhzad; Andrew S. Neish; Asma Nusrat

Annexin A1 released from epithelial extracellular vesicles and synthetic nanoparticles promotes wound repair

Miguel Quiros, Giovanna Leoni, Nazila Kamaly, Philipp-Alexander Neumann, Hikaru Nishio, Gabrielle Fredman, Mohammad Alam, Dennis Kusters, Chris Reutelingsperger, Mauro Perretti, Charles A. Parkos, Omid C. Farokhzad, Andrew S. Neish, Asma Nusrat

Research output: Contribution to journal › Conference abstract in journal › Research › peer-review

Abstract

Repair of epithelial wounds is essential for establishing intestinal mucosal homeostasis. Annexin 1 (AnxA1) promotes wound closure by activating intestinal epithelial formyl peptide receptor signaling. Here we show that AnxA1 is released from intestinal epithelial cells in extracellular vesicles (EVs). We determined that AnxA1 EV release is regulated by actin cytoskeletal dynamics and Rho GTPase signaling. EVs isolated from supernatants of epithelial cells increased reactive oxygen species generation and wound healing. Interestingly, EVs from AnxA1 null mice failed to enhance wound repair, demonstrating an important role of AnxA1 EVs in wound healing. Localized intramucosal administration of synthetic nanoparticles containing AnxA1 mimetic peptide Ac2-26 similarly promoted colonic mucosal wound repair. Epithelial derived AnxA1 EVs represent a novel mechanism regulating wound repair and local administration of synthetic vesicles containing pro-resolving peptides offer new therapeutic approaches to promote healing of intestinal mucosal ulcers

Original language	English
Journal	F A S E B Journal
Volume	28
Issue number	1
Pages (from-to)	1215-1227
ISSN	0892-6638
Publication status	Published - 2014
Externally published	Yes
Event	Experimental Biology 2014: Transforming the Future through Science - San Diego, United States Duration: 26 Apr 2014 → 30 Apr 2014

Conference

Conference	Experimental Biology 2014
Country/Territory	United States
City	San Diego
Period	26/04/2014 → 30/04/2014

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Quiros, M., Leoni, G., Kamaly, N., Neumann, P-A., Nishio, H., Fredman, G., Alam, M., Kusters, D., Reutelingsperger, C., Perretti, M., Parkos, C. A., Farokhzad, O. C., Neish, A. S., & Nusrat, A. (2014). Annexin A1 released from epithelial extracellular vesicles and synthetic nanoparticles promotes wound repair. F A S E B Journal, 28(1), 1215-1227. http://www.fasebj.org/content/28/1_Supplement/488.5

@article{9b053a53945b4994bf42bd82de32ea3a,

title = "Annexin A1 released from epithelial extracellular vesicles and synthetic nanoparticles promotes wound repair",

abstract = "Repair of epithelial wounds is essential for establishing intestinal mucosal homeostasis. Annexin 1 (AnxA1) promotes wound closure by activating intestinal epithelial formyl peptide receptor signaling. Here we show that AnxA1 is released from intestinal epithelial cells in extracellular vesicles (EVs). We determined that AnxA1 EV release is regulated by actin cytoskeletal dynamics and Rho GTPase signaling. EVs isolated from supernatants of epithelial cells increased reactive oxygen species generation and wound healing. Interestingly, EVs from AnxA1 null mice failed to enhance wound repair, demonstrating an important role of AnxA1 EVs in wound healing. Localized intramucosal administration of synthetic nanoparticles containing AnxA1 mimetic peptide Ac2-26 similarly promoted colonic mucosal wound repair. Epithelial derived AnxA1 EVs represent a novel mechanism regulating wound repair and local administration of synthetic vesicles containing pro-resolving peptides offer new therapeutic approaches to promote healing of intestinal mucosal ulcers ",

author = "Miguel Quiros and Giovanna Leoni and Nazila Kamaly and Philipp-Alexander Neumann and Hikaru Nishio and Gabrielle Fredman and Mohammad Alam and Dennis Kusters and Chris Reutelingsperger and Mauro Perretti and Parkos, {Charles A.} and Farokhzad, {Omid C.} and Neish, {Andrew S.} and Asma Nusrat",

year = "2014",

language = "English",

volume = "28",

pages = "1215--1227",

journal = "F A S E B Journal",

issn = "0892-6638",

publisher = "Federation of American Societies for Experimental Biology",

number = "1",

note = "Experimental Biology 2014 : Transforming the Future through Science ; Conference date: 26-04-2014 Through 30-04-2014",

}

Quiros, M, Leoni, G, Kamaly, N, Neumann, P-A, Nishio, H, Fredman, G, Alam, M, Kusters, D, Reutelingsperger, C, Perretti, M, Parkos, CA, Farokhzad, OC, Neish, AS & Nusrat, A 2014, 'Annexin A1 released from epithelial extracellular vesicles and synthetic nanoparticles promotes wound repair', F A S E B Journal, vol. 28, no. 1, pp. 1215-1227. <http://www.fasebj.org/content/28/1_Supplement/488.5>

TY - ABST

T1 - Annexin A1 released from epithelial extracellular vesicles and synthetic nanoparticles promotes wound repair

AU - Quiros, Miguel

AU - Leoni, Giovanna

AU - Kamaly, Nazila

AU - Neumann, Philipp-Alexander

AU - Nishio, Hikaru

AU - Fredman, Gabrielle

AU - Alam, Mohammad

AU - Kusters, Dennis

AU - Reutelingsperger, Chris

AU - Perretti, Mauro

AU - Parkos, Charles A.

AU - Farokhzad, Omid C.

AU - Neish, Andrew S.

AU - Nusrat, Asma

PY - 2014

Y1 - 2014

N2 - Repair of epithelial wounds is essential for establishing intestinal mucosal homeostasis. Annexin 1 (AnxA1) promotes wound closure by activating intestinal epithelial formyl peptide receptor signaling. Here we show that AnxA1 is released from intestinal epithelial cells in extracellular vesicles (EVs). We determined that AnxA1 EV release is regulated by actin cytoskeletal dynamics and Rho GTPase signaling. EVs isolated from supernatants of epithelial cells increased reactive oxygen species generation and wound healing. Interestingly, EVs from AnxA1 null mice failed to enhance wound repair, demonstrating an important role of AnxA1 EVs in wound healing. Localized intramucosal administration of synthetic nanoparticles containing AnxA1 mimetic peptide Ac2-26 similarly promoted colonic mucosal wound repair. Epithelial derived AnxA1 EVs represent a novel mechanism regulating wound repair and local administration of synthetic vesicles containing pro-resolving peptides offer new therapeutic approaches to promote healing of intestinal mucosal ulcers

AB - Repair of epithelial wounds is essential for establishing intestinal mucosal homeostasis. Annexin 1 (AnxA1) promotes wound closure by activating intestinal epithelial formyl peptide receptor signaling. Here we show that AnxA1 is released from intestinal epithelial cells in extracellular vesicles (EVs). We determined that AnxA1 EV release is regulated by actin cytoskeletal dynamics and Rho GTPase signaling. EVs isolated from supernatants of epithelial cells increased reactive oxygen species generation and wound healing. Interestingly, EVs from AnxA1 null mice failed to enhance wound repair, demonstrating an important role of AnxA1 EVs in wound healing. Localized intramucosal administration of synthetic nanoparticles containing AnxA1 mimetic peptide Ac2-26 similarly promoted colonic mucosal wound repair. Epithelial derived AnxA1 EVs represent a novel mechanism regulating wound repair and local administration of synthetic vesicles containing pro-resolving peptides offer new therapeutic approaches to promote healing of intestinal mucosal ulcers

M3 - Conference abstract in journal

SN - 0892-6638

VL - 28

SP - 1215

EP - 1227

JO - F A S E B Journal

JF - F A S E B Journal

IS - 1

T2 - Experimental Biology 2014

Y2 - 26 April 2014 through 30 April 2014

ER -

Annexin A1 released from epithelial extracellular vesicles and synthetic nanoparticles promotes wound repair

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