gms | German Medical Science

102. Jahrestagung der DOG

Deutsche Ophthalmologische Gesellschaft e. V.

23. bis 26.09.2004, Berlin

CTGF is the fibrogenic mediator of TGF-β in PVR disease

Meeting Abstract

  • corresponding author U. Welge-Lüßen - Augenklinik der Ludwig-Maximilians Universität, München
  • R. Fuchshofer - Anatomie II der Friedrich-Alexander Universität, Erlangen
  • A. Kampik - Augenklinik der Ludwig-Maximilians Universität, München

Evidenzbasierte Medizin - Anspruch und Wirklichkeit. 102. Jahrestagung der Deutschen Ophthalmologischen Gesellschaft. Berlin, 23.-26.09.2004. Düsseldorf, Köln: German Medical Science; 2004. Doc04dogDO.17.09

The electronic version of this article is the complete one and can be found online at:

Published: September 22, 2004

© 2004 Welge-Lüßen et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.




Proliferative vitreoretinopathy (PVR) is characterized by the formation of membranes. The extracellular matrix, like fibronectin, of these membranes is mainly formed by detached retinal pigment epithelial (RPE) cells. A previous study has shown that treatment of cultured RPE cells with transforming growth factor-beta2 (TGF-β2), a growth factor known to be increased in the vitreous of PVR patients, not only increased the amount of fibronectin but also lead to a irreversible crosslinking of this component by the enzyme tissue transglutaminase (tTG). As TGF-β2 is the most relevant factor for the immune privilege of the eye, a direct inhibition of TGF-β is obsolete. It is known, that the fibrogenic effect of TGF-β is mediated through connective tissue factor (CTGF). The goal of the present study was to investigate, whether the reduction of CTGF by siRNA inhibits the fibrogenic effect of TGF-β.


Monolayer cultures of RPE cells from eyes of 5 human donors were treated with 4.0 ng/ml TGF-β2, recombinant CTGF und CTGF siRNA fo 24-48 hours. Induction of fibronectin and tTG were investigated by western- and northern-blot analysis. External tTG activity was measured by incorporation of biotinylated cadaverine into fibronectin.


Treatment of cultured RPE cells with TGF-β2 increased the mRNA and protein levels of fibronectin 4-8 times. Additional TGF-β treatment increased tTG about the factor 4-6x. The increased expression correlated with an increased external tTG activity and irreversible polymerization of fibronectin. This effect was not seen by parallel treatment of TGF-β and CTGF siRNA. Treatment with recombinant CTGF showed similar results for fibronectin and tTG expression as treatment with TGF-β2.


CTGF is the fibrogenic mediator of TGF-β in PVR disease. Therefore the clinical use of CTGF inhibitor could help to prevent the PVR formation without affecting the immune privilege of the eye.