Regulation of Connective Tissue Growth Factor Expression Influences the Cell Viability In Human Trabecular Meshwork Cells

URN to cite this document:

urn:nbn:de:bvb:355-epub-313629 Copy

DOI to cite this document:

10.5283/epub.31362 Copy

Fuchsdorfer, Rudolf ; Tamm, Ernst R. ; Küspert, Sabrina Angela ; Braunger, Barbara Maria ; Junglas, Benjamin

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Date of publication of this fulltext: 26 Feb 2015 08:01

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Details

Item type:	Article
Journal or Publication Title:	Journal of Cellular and Molecular Medicine
Publisher:	Wiley Open Access
Volume:	19
Number of Issue or Book Chapter:	5
Page Range:	pp. 1010-1020
Date:	20 February 2015
Institutions:	Biology, Preclinical Medicine > Institut für Anatomie > Lehrstuhl für Humananatomie und Embryologie > Prof. Dr. Ernst Tamm
Projects:	Open Access Publizieren (DFG)
Identification Number:	Value Type 10.1111/jcmm.12492 DOI
Keywords:	CTGF ; glaucoma; trabecular meshwork; endothelin-1; angiotensin-II; IGF-1; oxidative stress; heat shock; αB-crystallin; cell viability
Dewey Decimal Classification:	500 Science > 570 Life sciences
Status:	Published
Refereed:	Yes, this version has been refereed
Created at the University of Regensburg:	Yes
Item ID:	31362

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Abstract

Connective tissue growth factor (CTGF) induces extracellular matrix (ECM) synthesis and contractility in human trabecular meshwork (HTM) cells. Both processes are involved in the pathogenesis of primary open-angle glaucoma. To date, little is known about regulation and function of CTGF expression in the trabecular meshwork (TM). Therefore, we analysed the effects of different aqueous humour ...

Abstract

Connective tissue growth factor (CTGF) induces extracellular matrix (ECM) synthesis and contractility in human trabecular meshwork (HTM) cells. Both processes are involved in the pathogenesis of primary open-angle glaucoma. To date, little is known about regulation and function of CTGF expression in the trabecular meshwork (TM). Therefore, we analysed the effects of different aqueous humour proteins and stressors on CTGF expression in HTM cells. HTM cells from three different donors were treated with endothelin-1, insulin-like growth factor (IGF)-1, angiotensin-II, H2O2 and heat shock and were analysed by immunohistochemistry, real-time RT-PCR and Western blotting. Viability after H2O2 treatment was measured in CTGF silenced HTM-N cells and their controls. Latrunculin A reduced expression of CTGF by about 50% compared to untreated HTM cells, whereas endothelin-1, IGF-1, angiotensin-II, heat shock and oxidative stress led to a significant increase. Silencing of CTGF resulted in a delayed expression of αB-crystallin and in reduced cell viability in comparison to the controls after oxidative stress. Conversely, CTGF treatment led to a higher cell viability rate after H2O2 treatment. CTGF expression is induced by factors that have been linked to glaucoma. An increased level of CTGF appears to protect TM cells against damage induced by stress. The beneficial effect of CTGF for viability of TM cells is likely associated with the effects on increased ECM synthesis and higher contractility of the TM, thereby contributing to reduced aqueous humour outflow facility causing increased intraocular pressure.

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Metadata last modified: 26 Nov 2020 00:22

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