A secreted collagen and fibronectin-binding streptococcal protein modulates cell-mediated collagen gel contraction and interstitial fluid pressure
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1143239
- author
- Liden, Åsa ; van Wieringen, Tijs ; Lannergard, Jonas ; Kassner, Anja LU ; Heinegård, Dick LU ; Reed, Rolf K ; Guss, Bengt and Rubin, Kristofer
- organization
- publishing date
- 2008
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Journal of Biological Chemistry
- volume
- 283
- issue
- 3
- pages
- 1234 - 1242
- publisher
- American Society for Biochemistry and Molecular Biology
- external identifiers
-
- pmid:18003607
- wos:000252282700006
- scopus:38349140674
- ISSN
- 1083-351X
- DOI
- 10.1074/jbc.M704827200
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Connective Tissue Biology (013230151)
- id
- c3734b4e-033a-4b05-b21e-afd8d0174c5a (old id 1143239)
- date added to LUP
- 2016-04-01 12:22:00
- date last changed
- 2022-03-13 08:55:54
@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 = {{American Society for Biochemistry and Molecular Biology}}, 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}}, doi = {{10.1074/jbc.M704827200}}, volume = {{283}}, year = {{2008}}, }