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A secreted collagen and fibronectin-binding streptococcal protein modulates cell-mediated collagen gel contraction and interstitial fluid pressure

Liden, Åsa; van Wieringen, Tijs; Lannergard, Jonas; Kassner, Anja LU ; Heinegård, Dick LU ; Reed, Rolf K; Guss, Bengt and Rubin, Kristofer (2008) In Journal of Biological Chemistry 283(3). p.1234-1242
Abstract
Fibroblast-mediated collagen gel contraction depends on collagen-binding ss1 integrins. Perturbation of these integrins reveals an alternative contraction process that is integrin aVss3-dependent and platelet-derived growth factor (PDGF) BB-stimulated. Connective tissue cells actively control interstitial fluid pressure (IFP) and inflammation-induced lowering of IFP provides a driving force for edema formation. PDGF-BB normalizes a lowered IFP by an aVss3-dependent process. A potential modulation of IFP by extracellular matrix-binding bacterial proteins has previously not been addressed. The fibronectin (FN) -binding protein FNE is specifically secreted by the highly virulent Streptococcus equi subspecies equi. FNE bound FN and native... (More)
Fibroblast-mediated collagen gel contraction depends on collagen-binding ss1 integrins. Perturbation of these integrins reveals an alternative contraction process that is integrin aVss3-dependent and platelet-derived growth factor (PDGF) BB-stimulated. Connective tissue cells actively control interstitial fluid pressure (IFP) and inflammation-induced lowering of IFP provides a driving force for edema formation. PDGF-BB normalizes a lowered IFP by an aVss3-dependent process. A potential modulation of IFP by extracellular matrix-binding bacterial proteins has previously not been addressed. The fibronectin (FN) -binding protein FNE is specifically secreted by the highly virulent Streptococcus equi subspecies equi. FNE bound FN and native collagen type I with Kd:s of ~20 and ~50 nM determined by solid-phase binding assays. Rotary shadowing revealed a single FNE-binding site located at on average 122 nm from the C-terminus of procollagen type I. FNE induced aVss3-mediated contraction by C2C12 cells in a concentration-dependent manner having a maximal effect at ~100 nM. This activity of FNE required cellular FN, and FNE acted synergistically to added plasma FN or PDGF-BB. FNE enhanced binding of soluble FN to immobilized collagen, and conversely the binding of collagen to immobilized FN. Marked bell-shaped concentration dependences for these interactions suggest that FNE forms a bridge between FN and collagen. Finally, FNE normalized dermal IFP lowered by anaphylaxis. Our data suggest that secreted FNE normalized lowering of IFP by stimulating connective tissue cell contraction. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Biological Chemistry
volume
283
issue
3
pages
1234 - 1242
publisher
ASBMB
external identifiers
  • pmid:18003607
  • wos:000252282700006
  • scopus:38349140674
ISSN
1083-351X
DOI
10.1074/jbc.M704827200
language
English
LU publication?
yes
id
c3734b4e-033a-4b05-b21e-afd8d0174c5a (old id 1143239)
date added to LUP
2008-07-30 14:16:17
date last changed
2017-07-30 03:48:55
@article{c3734b4e-033a-4b05-b21e-afd8d0174c5a,
  abstract     = {Fibroblast-mediated collagen gel contraction depends on collagen-binding ss1 integrins. Perturbation of these integrins reveals an alternative contraction process that is integrin aVss3-dependent and platelet-derived growth factor (PDGF) BB-stimulated. Connective tissue cells actively control interstitial fluid pressure (IFP) and inflammation-induced lowering of IFP provides a driving force for edema formation. PDGF-BB normalizes a lowered IFP by an aVss3-dependent process. A potential modulation of IFP by extracellular matrix-binding bacterial proteins has previously not been addressed. The fibronectin (FN) -binding protein FNE is specifically secreted by the highly virulent Streptococcus equi subspecies equi. FNE bound FN and native collagen type I with Kd:s of ~20 and ~50 nM determined by solid-phase binding assays. Rotary shadowing revealed a single FNE-binding site located at on average 122 nm from the C-terminus of procollagen type I. FNE induced aVss3-mediated contraction by C2C12 cells in a concentration-dependent manner having a maximal effect at ~100 nM. This activity of FNE required cellular FN, and FNE acted synergistically to added plasma FN or PDGF-BB. FNE enhanced binding of soluble FN to immobilized collagen, and conversely the binding of collagen to immobilized FN. Marked bell-shaped concentration dependences for these interactions suggest that FNE forms a bridge between FN and collagen. Finally, FNE normalized dermal IFP lowered by anaphylaxis. Our data suggest that secreted FNE normalized lowering of IFP by stimulating connective tissue cell contraction.},
  author       = {Liden, Åsa and van Wieringen, Tijs and Lannergard, Jonas and Kassner, Anja and Heinegård, Dick and Reed, Rolf K and Guss, Bengt and Rubin, Kristofer},
  issn         = {1083-351X},
  language     = {eng},
  number       = {3},
  pages        = {1234--1242},
  publisher    = {ASBMB},
  series       = {Journal of Biological Chemistry},
  title        = {A secreted collagen and fibronectin-binding streptococcal protein modulates cell-mediated collagen gel contraction and interstitial fluid pressure},
  url          = {http://dx.doi.org/10.1074/jbc.M704827200},
  volume       = {283},
  year         = {2008},
}