Nineteen cases of epiretinal membrane (ERM) in proliferative diabetic retinopathy were studied using immunohistochemical methods. Antibodies against type I-IV collagen, fibronectin (FN), glial fibrillary acidic protein (GFAP), vimentin and the monoclonal antibody (MAB) against human Müller cells were used to examine the membranes. Type II collagen was found on one side of the ERMs in 95% of the cases. The other types of collagen, FN and vimentin were also identified in most cases. Müller cells (GFAP- and MAB-positive) were found in 2/19 cases (11 %), and astrocytes (GFAP-positive but MAB-negative) were found in 10/19 cases (53%). These results suggest that type II collagen (vitreal collagen) may act as a scaffolding in the formation of ERMs and that glial elements of the ERMs consist mainly of astrocytes.
Intravitreal neovascular tissue in 8 cases of proliferative diabetic retinopathy was investigated using immunohistochemical techniques. All 8 cases yielded positive immuno reactivity for type II collagen (vitreous collagen). The intravitreal neovascular tissue was classified into two groups (A or B), depending upon the distribution of type II collagen. In group A (3 cases), blood vessels were entirely surrounded by vitreous collagen, and in group B (5 cases), the vessels proliferated on one side of a mass of vitreous collagen. Type I and III collagens were distributed diffusely within the extracellular space of the tissue, whereas type IV collagen and fibronectin (FN) formed a basement membrane-like foundation for the newly formed vessels. Glial fibrillary acidic protein (GFAP)-immunoreactive cells were not clearly detected in any of the cases. Neovascular tissue typically proliferated on the posterior vitreous surface (as found in group B), but was also found to penetrate the vitreous gel (as found in group A). As neovascular tissue proliferation proceeded, types I, III and IV collagens and FN were produced. Glial cells (GFAP-positive cells) were not essential for neovascular tissue formation.
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