Abstract
Purpose: :
To assess the potential contributions of retinal Müller cells to tractional force generation in proliferative diabetic retinopathy.
Methods: :
Diabetic epiretinal tissues (six) were cryosectioned and probed with antibodies against known Müller cell and myoid proteins including glial fibrillary acid protein (GFAP), Vimentin, Glutamine Synthetase and alpha Smooth Muscle Actin (αSMA). Temporal changes in expression of these antigens were also evaluated in cultures of freshly isolated porcine Müller cells using indirect immunofluorescence and Western blotting.
Results: :
All six samples contained cells GFAP + Vimentin-positive and GFAP + Glutamine Synthetase-positive cells identifiable as of Müller cell origin. There appeared to be a progressive loss of Glutamine Synthetase and GFAP content as the cells assumed an elongate, fibroblast-like morphology. Vimentin expression did not change. Müller cells with progressive increases in aSMA content were also detected in all samples. The same progression of antigen changes was observed in cultures of freshly isolated Müller cells.
Conclusions: :
Müller cells are present in diabetic epiretinal tissues, undergo the same progression of phenotype changes described for cells in culture and contribute to the population of tractional force generating cells that cause retinal detachment.
Keywords: diabetic retinopathy • Muller cells • retinal detachment