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Integrin αVβ3 can substitute for collagen‐binding β1‐integrins in vivo to maintain a homeostatic interstitial fluid pressure
Univ Bergen, Dept Biomed, Bergen, Norway.
Univ Bergen, Dept Biomed, Bergen, Norway.
Swedish Univ Agr Sci, Dept Biomed Sci & Vet Publ Hlth, Uppsala, Sweden.
Univ Bergen, Dept Biomed, Bergen, Norway; Univ Bergen, Ctr Canc Biomarkers CCBIO, Bergen, Norway.
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2018 (English)In: Experimental Physiology, ISSN 0958-0670, E-ISSN 1469-445X, Vol. 103, no 5, p. 629-634Article in journal (Refereed) Published
Abstract [en]

Accumulated data indicate that cell‐mediated contraction of reconstituted collagenous gels in vitro can serve as a model for cell‐mediated control of interstitial fluid pressure (PIF) in vivo. A central role for collagen‐binding β1‐integrins in both processes has been established. Furthermore, integrin αVβ3 takes over the role of collagen‐binding β1‐integrins in mediating contraction after perturbations of collagen‐binding β1‐integrins in vitro. Integrin αVβ3 is also instrumental for normalization of dermal PIF that has been lowered due to mast cell degranulation with compound 48/80 (C48/80) in vivo. Here we demonstrate a role of integrin αVβ3 in maintaining a long term homeostatic dermal PIF in mice lacking the collagen‐binding integrin  α11β1 (α11−/− mice). Measurements of PIF were performed after circulatory arrest. Furthermore, cell‐mediated integrin αVβ3‐directed contraction of collagenous gels in vitro depends on free access to a collagen site known to bind several extracellular matrix (ECM) proteins that form substrates for αVβ3‐directed cell attachment, such as fibronectin and fibrin. A streptococcal collagen‐binding protein, CNE, specifically binds to and blocks this site on the collagen triple helix. Here we show that whereas CNE perturbed αVβ3‐directed and platelet‐derived growth factor BB‐induced normalization of dermal PIF after C48/80, it did not affect αVβ3‐dependent maintenance of a homeostatic dermal PIF. These data imply that dynamic modification of the ECM structure is needed during acute patho‐physiological modulations of PIF but not for long‐term maintenance of a homeostatic PIF. Our data thus show that collagen‐binding β1‐integrins, integrin αVβ3 and ECM structure are potential targets for novel therapy aimed at modulating oedema formation and hypovolemic shock during anaphylaxis.

Place, publisher, year, edition, pages
2018. Vol. 103, no 5, p. 629-634
Keywords [en]
contraction, extracellular matrix, microcirculation
National Category
Biochemistry and Molecular Biology
Identifiers
URN: urn:nbn:se:uu:diva-356075DOI: 10.1113/EP086902ISI: 000431497300002PubMedID: 29524327OAI: oai:DiVA.org:uu-356075DiVA, id: diva2:1232959
Funder
Swedish Research CouncilSwedish Research Council FormasSwedish Cancer Society
Note

WoS title: Integrin alpha(V)beta(3) can substitute for collagen-binding beta(1)-integrins in vivo to maintain a homeostatic interstitial fluid pressurel

Available from: 2018-07-13 Created: 2018-07-13 Last updated: 2018-07-13Bibliographically approved

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