April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Understanding The Biology Of The Stromal Myofibroblasts That Contribute To Opacity Following Corneal Injury
Author Affiliations & Notes
  • Flavia L. Barbosa
    Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, Ohio
  • Marcony R. Santhiago
    Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, Ohio
  • Vivek Singh
    Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, Ohio
  • Vandana Agrawal
    Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, Ohio
  • Steven E. Wilson
    Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, Ohio
  • Footnotes
    Commercial Relationships  Flavia L. Barbosa, None; Marcony R. Santhiago, None; Vivek Singh, None; Vandana Agrawal, None; Steven E. Wilson, None
  • Footnotes
    Support  EY10056 and EY15638 from National Eye Institute, National Institutes of Health, Bethesda, Maryland and Research to Prevent Blindness, New York, NY.
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 5304. doi:
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    • Get Citation

      Flavia L. Barbosa, Marcony R. Santhiago, Vivek Singh, Vandana Agrawal, Steven E. Wilson; Understanding The Biology Of The Stromal Myofibroblasts That Contribute To Opacity Following Corneal Injury. Invest. Ophthalmol. Vis. Sci. 2011;52(14):5304.

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

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Abstract
 
Purpose:
 

To investigate the role of interleukin-1 (IL-1) in modulating myofibroblast viability in mice corneas with haze induced by irregular phototherapeutic keratectomy (PTK).

 
Methods:
 

female B6;129S1-Il1r1tm1Roml/J homozygous IL-1RI knockout mice and control B6129SF2/J mice were included in this study. Haze-generating irregular phototherapeutic keratectomy (PTK) was performed in one eye. Mice were euthanized at 1 month and 6 months after surgery and the eyes were cryo-preserved in OCT. The contralateral eye served as unwounded control. There were four eyes in each group at each time point. Immunohistochemistry was performed for α-smooth muscle actin (SMA) and vimentin (Vim) in the unwounded and wounded corneas.

 
Results:
 

No stromal SMA was detected in the stroma of unwounded corneas. SMA+ myofibroblast density was significantly higher in the IL-1RI knockout group than the control group at 1 month (1.6±0.2 and 0.7±0.1, respectively) and at 6 months (1.1±0.2 and 0.3±0.1, respectively, table). More vimentin+ cells were detected in the stroma of unwounded Il-1R knockout corneas than unwounded control corneas at 1 month (9.5±0.1 and 6.5±0.4, respectively) and at 6 months (9.06±0.4 and 6.06±0.3, respectively). These differences were significant (p< 0.01).

 
Conclusions:
 

Recent in vitro work has demonstrated an antagonistic effect of TGFβ and IL-1 on myofibroblast viability and discovered- IL-1 effects in promoting myofibroblast apoptosis are suppressed by TGFβ. This in situ study confirms that IL-1 is an important modulator of myofibroblast viability during corneal wound healing and that IL-1 may have a role in suppressing vim+ SMA- myofibroblast precursors when stromal levels of TGFβ are low.  

 
Keywords: cornea: stroma and keratocytes • inflammation • refractive surgery: complications 
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