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 journalConference abstract in journalResearchpeer-review


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 languageEnglish
JournalF A S E B Journal
Issue number1
Pages (from-to)1215-1227
Publication statusPublished - 2014
Externally publishedYes
EventExperimental Biology 2014: Transforming the Future through Science - San Diego, United States
Duration: 26 Apr 201430 Apr 2014


ConferenceExperimental Biology 2014
Country/TerritoryUnited States
CitySan Diego


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