Context-Dependent Role of Vinculin in Neutrophil Adhesion, Motility and Trafficking.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
07 02 2020
Historique:
received: 25 11 2019
accepted: 22 01 2020
entrez: 9 2 2020
pubmed: 9 2 2020
medline: 11 11 2020
Statut: epublish

Résumé

Neutrophils are innate immune effector cells that traffic from the circulation to extravascular sites of inflammation. β2 integrins are important mediators of the processes involved in neutrophil recruitment. Although neutrophils express the cytoskeletal protein vinculin, they do not form mature focal adhesions. Here, we characterize the role of vinculin in β2 integrin-dependent neutrophil adhesion, migration, mechanosensing, and recruitment. We observe that knockout of vinculin attenuates, but does not completely abrogate, neutrophil adhesion, spreading, and crawling under static conditions. However, we also found that vinculin deficiency does not affect these behaviors in the presence of forces from fluid flow. In addition, we identify a role for vinculin in mechanosensing, as vinculin-deficient neutrophils exhibit attenuated spreading on stiff, but not soft, substrates. Consistent with these findings, we observe that in vivo neutrophil recruitment into the inflamed peritoneum of mice remains intact in the absence of vinculin. Together, these data suggest that while vinculin regulates some aspects of neutrophil adhesion and spreading, it may be dispensable for β2 integrin-dependent neutrophil recruitment in vivo.

Identifiants

pubmed: 32034208
doi: 10.1038/s41598-020-58882-y
pii: 10.1038/s41598-020-58882-y
pmc: PMC7005776
doi:

Substances chimiques

CD18 Antigens 0
Vinculin 125361-02-6

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

2142

Subventions

Organisme : NIDCR NIH HHS
ID : F31 DE028745
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI116629
Pays : United States
Organisme : NIGMS NIH HHS
ID : R35 GM124911
Pays : United States

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Auteurs

Zachary S Wilson (ZS)

Graduate Program in Pathobiology, Brown University, Providence, RI, 02912, USA.
Department of Surgery, Division of Surgical Research, Rhode Island Hospital, Providence, RI, 02903, USA.

Hadley Witt (H)

Graduate Program in Pathobiology, Brown University, Providence, RI, 02912, USA.
Department of Surgery, Division of Surgical Research, Rhode Island Hospital, Providence, RI, 02903, USA.

Lauren Hazlett (L)

School of Engineering, Brown University, Providence, RI, 02912, USA.

Michael Harman (M)

Department of Surgery, Division of Surgical Research, Rhode Island Hospital, Providence, RI, 02903, USA.
School of Engineering, Brown University, Providence, RI, 02912, USA.

Brittany M Neumann (BM)

Department of Surgery, Division of Surgical Research, Rhode Island Hospital, Providence, RI, 02903, USA.

Andrew Whitman (A)

Department of Surgery, Division of Surgical Research, Rhode Island Hospital, Providence, RI, 02903, USA.

Mohak Patel (M)

School of Engineering, Brown University, Providence, RI, 02912, USA.

Robert S Ross (RS)

University of California San Diego, School of Medicine, Department of Medicine/Cardiology, La Jolla, CA, 92093, USA.

Christian Franck (C)

Department of Mechanical Engineering, University of Wisconsin-Madison, Madison, WI, 53706, USA.

Jonathan S Reichner (JS)

Department of Surgery, Division of Surgical Research, Rhode Island Hospital, Providence, RI, 02903, USA.

Craig T Lefort (CT)

Department of Surgery, Division of Surgical Research, Rhode Island Hospital, Providence, RI, 02903, USA. craig_lefort@brown.edu.

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