June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Dexamethasone Modifies Viability of Mitomycin C-Treated Tenon’s Fibroblasts
Author Affiliations & Notes
  • Shu-Wen Chang
    Department of Ophthalmology, Far Eastern Memorial Hospital, New Taipei City, Taiwan
    Department of Ophthalmology, National Taiwan University Hospital, Taipei, Taiwan
  • Wei-Ting Ho
    Department of Ophthalmology, Far Eastern Memorial Hospital, New Taipei City, Taiwan
  • Tsan-Chi Chen
    Department of Ophthalmology, Far Eastern Memorial Hospital, New Taipei City, Taiwan
  • San-Fong Chou
    Department of Medical Research, Far Eastern Memorial Hospital, New Taipei City, Taiwan
  • Footnotes
    Commercial Relationships Shu-Wen Chang, None; Wei-Ting Ho, None; Tsan-Chi Chen, None; San-Fong Chou, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 5407. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Shu-Wen Chang, Wei-Ting Ho, Tsan-Chi Chen, San-Fong Chou; Dexamethasone Modifies Viability of Mitomycin C-Treated Tenon’s Fibroblasts. Invest. Ophthalmol. Vis. Sci. 2013;54(15):5407.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract
 
Purpose
 

To investigate whether dexamethasone modifies the effect of mitomycin C (MMC) in human Tenon’s capsule fibroblasts (HTFs) and to explore its molecular mechanism.

 
Methods
 

HTFs were treated with MMC for 5 minutes and incubated in DMEM with 10 μM dexamethasone (DEX). Viability of the treated HTFs was analyzed by WST-1 assay. The amount of IL-8 section in untreated, MMC-treated, or peroxisome proliferator-activated receptor gamma (PPARγ)-silenced HTFs was determined by enzyme-linked immunosorbent assay. Expression of PPARγ and the apoptotic proteins was examined by immunoblotting.

 
Results
 

Recombinant IL-8 noticeably suppressed HTF cell proliferation in a dose-dependent manner. MMC treatment significantly upregulated IL-8 secretion and inhibited cell proliferation in HTFs. Both effects were reversed by DEX incubation. DEX upregulated PPARγ and Bcl-xL in untreated HTFs and MMC-treated HTFs at 1 day and 2 days of incubation, respectively. PPARγ silencing reduced Bcl-xL expression and enhanced IL-8 secretion. However, MMC treatment and/or DEX incubation did not alter the expression of two apoptotic indicators, PARP-1 and pro-caspase-3.

 
Conclusions
 

DEX reversed the MMC-inhibited HTF cell proliferation and diminished the MMC-upregulated IL-8 secretion via upregulating the PPARγ expression (Figure 1).

 
 
Figure 1. Scheme depicting reverse regulation of dexamethasone in MMC-induced cell death of HTFs.
 
Figure 1. Scheme depicting reverse regulation of dexamethasone in MMC-induced cell death of HTFs.
 
Keywords: 449 cell survival • 490 cytokines/chemokines • 503 drug toxicity/drug effects  
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×