Predominance of MMP-1 and MMP-2 in Epiretinal and Subretinal Membranes of Proliferative Vitreoretinopathy

Positive Feedback Regulation between MMP-9 and VEGF in Human RPE Cells

“…[15][16][17][18] These proteinases degrade-in addition to many nonmatrix molecules-most extracellular matrix components including type IV collagen, a major component of basement membranes and Bruch membrane, thereby allowing proteolysis-associated migration of endothelial cells. MMP-2 and MMP-9 have been implicated in the induction of retinal neovascularization in the retinopathy of prematurity animal model, in the pathogenesis of diabetic retinopathy, and in choroidal neovascularization (CNV).…”

Pathobiology of epiretinal and subretinal membranes: possible roles for the matricellular proteins thrombospondin 1 and osteonectin (SPARC)

“…However, several other families of molecules are likely to be involved in controlling adhesive interactions between RPE cells and matrix, such as the matrix metalloproteinases (MMPs), and the metallodisintegrin (ADAM) and the ADAM with thrombospondin repeats (ADAMTS) families. [60][61][62][63] Indeed, it is established that RPE cells are capable of synthesising many of these proteins, [60][61][62][63] and that MMPs are required for some RPE cell-collagen matrix interactions like those which are involved in collagen matrix contraction. 64,65 In addition to separation from Bruch's membrane, RPE cells destined for the new PVR membranes have to detach from their neighbours.…”

Role of Retinal Detachment Subretinal Fluid on Extracellular Matrix Metabolism

“…However, a loss of ECM metabolism regulation occurs under particular conditions with an excessive deposit of ECM components such as collagen. Molecules involved in ECM synthesis and degradation like MMPs and some cytokines have been identified in normal and pathological vitreous as well as in the epiretinal and subretinal membranes of PVR patients [21, 22, 23]. These molecules could be carried out from the vitreous through the subretinal space during the evolution of retinal detachment [24].…”