PDGF-BB induces expression of LTBP-1 but not TGF-β1 in a rat cirrhotic fat storing cell line

TGF-β, a profibrogenic cytokine is predominantly secreted as a latent molecule complexed with one of the latent TGF-β binding proteins (LTBP). Due to the proposed functions of LTBP-1 and -3 in regulating TGF-β-bioavailability and -activity, we investigated the effects of PDGF-BB and TGF-β1 on their...

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Main Authors: Westhoff, Jens (Author) , Sawitza, Iris (Author) , Keski-Oja, Jorma (Author) , Gressner, Axel M. (Author) , Breitkopf-Heinlein, Katja (Author)
Format: Article (Journal)
Language:English
Published: 2003
In: Growth factors
Year: 2003, Volume: 21, Issue: 3/4, Pages: 121-130
ISSN:1029-2292
DOI:10.1080/08977190310001637224
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1080/08977190310001637224
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Author Notes:Jens H. Westhoff, Iris Sawitza, Jorma Keski-Oja, Axel M. Gressner & Katja Breitkopf
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Summary:TGF-β, a profibrogenic cytokine is predominantly secreted as a latent molecule complexed with one of the latent TGF-β binding proteins (LTBP). Due to the proposed functions of LTBP-1 and -3 in regulating TGF-β-bioavailability and -activity, we investigated the effects of PDGF-BB and TGF-β1 on their expression levels in Cirrhotic fat storing cells (CFSC). CFSC basally express LTBP-1 and -3 and TGF-β1. LTBP-1 colocalizes with LAP and the cells secrete some active TGF-β1. Promoter studies showed no strong induction of the LTBP-1 promoters after stimulation, although mRNA and protein levels were increased by PDGF-BB treatment without affecting TGF-β1 expression. Vice versa, TGF-β1 treatment did not alter LTBP-1 expression while an autocrine induction was found. Our data indicate that LTBP-1 but not TGF-β1 is induced by PDGF-BB and that TGF-β1 autoinduction does not affect the expression of LTBP-1. This divergent regulation may represent an important mechanism for modulation of TGF-β bioavailability.
Item Description:Elektronische Reproduktion der Druck-Ausgabe
Published online: 07 Aug 2009
Gesehen am 23.06.2022
Physical Description:Online Resource
ISSN:1029-2292
DOI:10.1080/08977190310001637224