Av. Ljubimov et al., EXTRACELLULAR-MATRIX ALTERATIONS IN HUMAN CORNEAS WITH BULLOUS KERATOPATHY, Investigative ophthalmology & visual science, 37(6), 1996, pp. 997-1007
Purpose. To uncover abnormalities of extracellular matrix (ECM) distri
bution in human corneas with pseudophakic and aphakic bullous keratopa
thy (PBK/ABK). Methods. Indirect immunofluorescence with antibodies to
27 ECM components was used on frozen sections of 14 normal and 20 PBK
/ABK corneas. Results. Fibrillar deposits of an antiadhesive glycoprot
ein tenascin in the anterior and posterior stroma, epithelial basement
membrane (BM), bullae and subepithelial fibrosis (SEF) areas, and pos
terior collagenous layer (PCL) were revealed in diseased corneas. Tena
scin in midstroma, which was observed in some cases, correlated with d
ecreased visual acuity. In normal central corneas, tenascin was never
found. Other major ECM abnormalities in PBK/ABK corneas compared to no
rmals included: discontinuous epithelial BM staining for laminin-1 (al
pha 1 beta 1 gamma 1), entactin/nidogen and fibronectin; accumulation
of fibronectin and alpha 1-alpha 2 type IV collagen on the endothelial
face of the Descemet's membrane; and abnormal deposition of stromal E
CM (tenascin, fibronectin, decorin, types I, III, V, VI, VIII, XII, XI
V collagen) and BM components (type IV collagen, perlecan, bamacan, la
minin-l, entactin-nidogen, fibronectin) in SEF areas and in PCL. Concl
usions. This study provides a molecular description of an ongoing fibr
osis on the epithelial, stromal, and endothelial levels in PBK/ABK cor
neas. These fibrotic changes may follow initial endothelial damage aft
er cataract surgery, may be caused by the upregulation of fibrogenic c
ytokines, and may play a significant role in the progression of bullou
s keratopathy.