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BY 4.0 license Open Access Published by De Gruyter November 26, 2020

Fibrosis: Altered gene expression in TGF-β stimulated human fibroblasts of the Tenon

  • Andreas Brietzke EMAIL logo , Rudolf Guthoff , Thomas Stahnke and Niels Grabow

Abstract

Despite decades of research, fibrosis still remains a significant challenge for medicine in many different fields. Although there is a general model of fibrosis, the causes and characteristics of the various pathologies are as diverse as the variety of organs and tissues that can be affected by fibrosis. Moreover, fibrosis also impedes the long-term prospects of success in implantation surgery. One possibility to address this challenge is the development of biocompatible implants featuring drug delivery systems loaded with antifibrotic pharmaceuticals. Due to diverse regulatory mechanisms in organs, tissues and also cell types, these active substances must consequentially be designed for diverse specific applications. Compared to fibrosis in organs like lung or liver, these mechanisms were poorly addressed in ophthalmologic research, but it is known that transforming growth factor beta (TGF-β) plays a key role. This gene expression study revealed 30 genes being upregulated more than two fold in TGF-β1 treated human primary tenon fibroblasts (hTF). Furthermore, 15 genes were found to be downregulated more than two fold. Tumor necrosis factor (TNF), vascular endothelial growth factor A (VEGFA) and inhibin beta (INHBE) were particular strongly regulated in TGF-β1 treated hTFs.

Published Online: 2020-11-26
Published in Print: 2020-09-01

© 2020 by Walter de Gruyter Berlin/Boston

This work is licensed under the Creative Commons Attribution 4.0 International License.

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