Regulation of fibroblast-mediated collagen gel contraction by platelet-derived growth factor, interleukin-1 alpha and transforming growth factor-beta 1
Författare
Summary, in English
We have examined the effects of three macrophagederived
cytokines, platelet-derived growth factor (PDGF), transforming growth factor-01 (TGF-01) and interleukin-1 a (IL-la) on the contraction of collagen type I gels populated by human foreskin fibroblasts. Contraction was quantified as loss in gel weight. Both PDGF-AA and PDGF-BB were found to induce a rapid collagen-gel contraction. TGF-/J1 also stimulated gel contraction but with a delayed onset and at a slower rate than the PDGF-stimulated contraction. Rabbit polyclonal IgGs recognizing PDGF-AA and PDGF-BB, respectively, specifically inhibited the effects of the corresponding PDGF Lsoforms. However, the stimulatory effect of TGF-/S1 was not affected by any of the anti-PDGF antibodies. The ability of PDGF to stimulate
contraction became less pronounced in collagen gel cultures grown in the absence of growth factors over periods of several days. Under the same conditions, the stimulatory effect of TGF-/J1 was not reduced. The reduced response to PDGF may be due to reduced tension on fibroblasts growing in collagen gels, since fibroblasts on free-floating gels showed a marked reduction in PDGF-BB-induced PDGF ^-receptor aggregates when compared to fibroblasts on attached collagen gels. LL-1 a inhibited initial collagen gel contraction, and at later stages induced a visible degradation of the collagen gels, presumably due to the generation of collagenase activity. The combination of IL-la and PDGF-BB stimulated initial collagen gel contraction, although less effectively than PDGF-BB alone. At later stages, collagen gel degradation was stimulated by this combination of cytokines. In contrast, the combination
of IL-la and TGF-/51 did not stimulate collagen gel
contraction, or any visible collagen gel degradation. Our
data suggest that fibroblast-mediated collagen gel contraction can be modulated by cytokines via different
mechanisms. Our data are of importance in the understanding of the modulatory roles of cytokines in connective tissue cell activities in inflammatory processes, such as wound healing.
cytokines, platelet-derived growth factor (PDGF), transforming growth factor-01 (TGF-01) and interleukin-1 a (IL-la) on the contraction of collagen type I gels populated by human foreskin fibroblasts. Contraction was quantified as loss in gel weight. Both PDGF-AA and PDGF-BB were found to induce a rapid collagen-gel contraction. TGF-/J1 also stimulated gel contraction but with a delayed onset and at a slower rate than the PDGF-stimulated contraction. Rabbit polyclonal IgGs recognizing PDGF-AA and PDGF-BB, respectively, specifically inhibited the effects of the corresponding PDGF Lsoforms. However, the stimulatory effect of TGF-/S1 was not affected by any of the anti-PDGF antibodies. The ability of PDGF to stimulate
contraction became less pronounced in collagen gel cultures grown in the absence of growth factors over periods of several days. Under the same conditions, the stimulatory effect of TGF-/J1 was not reduced. The reduced response to PDGF may be due to reduced tension on fibroblasts growing in collagen gels, since fibroblasts on free-floating gels showed a marked reduction in PDGF-BB-induced PDGF ^-receptor aggregates when compared to fibroblasts on attached collagen gels. LL-1 a inhibited initial collagen gel contraction, and at later stages induced a visible degradation of the collagen gels, presumably due to the generation of collagenase activity. The combination of IL-la and PDGF-BB stimulated initial collagen gel contraction, although less effectively than PDGF-BB alone. At later stages, collagen gel degradation was stimulated by this combination of cytokines. In contrast, the combination
of IL-la and TGF-/51 did not stimulate collagen gel
contraction, or any visible collagen gel degradation. Our
data suggest that fibroblast-mediated collagen gel contraction can be modulated by cytokines via different
mechanisms. Our data are of importance in the understanding of the modulatory roles of cytokines in connective tissue cell activities in inflammatory processes, such as wound healing.
Publiceringsår
1992
Språk
Engelska
Sidor
315-322
Publikation/Tidskrift/Serie
Journal of Cell Science
Volym
102
Issue
2
Dokumenttyp
Artikel i tidskrift
Förlag
The Company of Biologists Ltd
Ämne
- Cancer and Oncology
- Psychiatry
Nyckelord
- fibroblasts
- transforming growth factor-^3
- plateletderived growth factor
- interleukin-1
- collagen
Status
Published
Forskningsgrupp
- Psychiatric Neuromodulation Unit (PNU)
ISBN/ISSN/Övrigt
- ISSN: 0021-9533