Myeloid-derived growth factor regulates neutrophil motility in interstitial tissue damage.
Autor: | Houseright RA; Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, WI., Miskolci V; Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, WI., Mulvaney O; Department of Pediatrics, University of Wisconsin-Madison, Madison, WI., Bortnov V; Department of Biomolecular Chemistry, University of Wisconsin-Madison, Madison, WI., Mosher DF; Department of Biomolecular Chemistry, University of Wisconsin-Madison, Madison, WI., Rindy J; Department of Pediatrics, University of Wisconsin-Madison, Madison, WI., Bennin DA; Department of Pediatrics, University of Wisconsin-Madison, Madison, WI., Huttenlocher A; Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, WI.; Department of Pediatrics, University of Wisconsin-Madison, Madison, WI. |
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Jazyk: | angličtina |
Zdroj: | The Journal of cell biology [J Cell Biol] 2021 Aug 02; Vol. 220 (8). Date of Electronic Publication: 2021 May 28. |
DOI: | 10.1083/jcb.202103054 |
Abstrakt: | Neutrophil recruitment to tissue damage is essential for host defense but can also impede tissue repair. The cues that differentially regulate neutrophil responses to tissue damage and infection remain unclear. Here, we report that the paracrine factor myeloid-derived growth factor (MYDGF) is induced by tissue damage and regulates neutrophil motility to damaged, but not infected, tissues in zebrafish larvae. Depletion of MYDGF impairs wound healing, and this phenotype is rescued by depleting neutrophils. Live imaging and photoconversion reveal impaired neutrophil reverse migration and inflammation resolution in mydgf mutants. We found that persistent neutrophil inflammation in tissues of mydgf mutants was dependent on the HIF-1α pathway. Taken together, our data suggest that MYDGF is a damage signal that regulates neutrophil interstitial motility and inflammation through a HIF-1α pathway in response to tissue damage. (© 2021 Houseright et al.) |
Databáze: | MEDLINE |
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