June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Molecular Markers in Proliferative Diabetic Retinopathy
Author Affiliations & Notes
  • William Chang
    Ophthalmology, Northwestern University, Chicago, IL
  • Ronil S. Shah
    Ophthalmology, Northwestern University, Chicago, IL
  • Michelle Lajko
    Ophthalmology, Northwestern University, Chicago, IL
  • Amani A Fawzi
    Ophthalmology, Northwestern University, Chicago, IL
  • Footnotes
    Commercial Relationships William Chang, None; Ronil Shah, None; Michelle Lajko, None; Amani Fawzi, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 5197. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to Subscribers Only
      Sign In or Create an Account ×
    • Get Citation

      William Chang, Ronil S. Shah, Michelle Lajko, Amani A Fawzi; Molecular Markers in Proliferative Diabetic Retinopathy. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):5197.

      Download citation file:


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

      ×
  • Supplements
Abstract
 
Purpose
 

Proliferative diabetic retinopathy (PDR) is a late stage manifestation of diabetic retinopathy characterized by neovascularization, fibrosis, and the formation of an epiretinal membrane (ERM). The exact molecular mechanisms of PDR membrane formation remain unclear. We used immunohistochemical methods to study the cellular composition and unique molecular markers in PDR ERMs versus idiopathic ERMs.

 
Methods
 

ERMs were obtained from patients undergoing pars plana vitrectomy. ERMs were designated as either PDR-related or idiopathic based on the patient’s history prior to vitrectomy. All collected ERMs were cryo-protected, fixed in paraformaldehyde, and cryo-sectioned. The sectioned membranes were stained with glial fibrillary protein (GFAP), alpha-smooth muscle actin (SMA), and isolectin-IB4 (IB4), markers for retinal glial cells, myofibroblasts, and vascular endothelial cells, respectively. Control slides without primary antibodies were made for each immunostain. Immunoreactivity of each marker was visualized using fluorescent light microscopy.

 
Results
 

SMA and GFAP immunoreactivity is seen primarily in the cytoplasm of cells in PDR ERMs while IB4 immunoreactivity is localized in the stromal region of PDR ERMs. Qualitative imaging suggests that SMA and IB4 immunoreactivities are increased in ERMs from PDR patients compared to idiopathic ERM. In contrast, GFAP immunoreactivity appears to be prominent in both PDR and idiopathic ERMs, suggesting similar involvement of glial cells in both ERM types

 
Conclusions
 

Myofibroblasts and vascular endothelial cells are major components of ERMs in PDR and appear to be involved in the formation of ERMs in diabetes, while glial cells are expressed in both idiopathic and diabetic ERMs. This research may further elucidate the role of various molecular markers in PDR membranes and provide new targets for therapeutic interventions.  

 
Immunohistochemistry staining of SMA and IB4 in ERMs (7 μm sections; magnification x20). The top panels are of the same ERM section from a patient without PDR. The bottom panels are of the same ERM section from a patient with PDR. DAPI stains cell nuclei.
 
Immunohistochemistry staining of SMA and IB4 in ERMs (7 μm sections; magnification x20). The top panels are of the same ERM section from a patient without PDR. The bottom panels are of the same ERM section from a patient with PDR. DAPI stains cell nuclei.

 
×
×

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.

×