Effect of Vitreous on Morphologic Characteristics of Retinal Pigment Epithelial Cells

Non-Paralleled Increase of Hepatocyte Growth Factor and Vascular Endothelial Growth Factor in the Eyes with Angiogenic and Nonangiogenic Fibroproliferation

“…In PVR, the RPE cells proliferate and migrate as soon as the neural retina detaches from the RPE layer. These cells frequently lack pigment granules and exhibit a macrophage or fibroblast-like morphologic phenotype [35]. Recently, it was reported that RPE cell shape transformed to a more fibroblast-like appearance in the presence of HGF and c-Met in vitro [36].…”

Non-Paralleled Increase of Hepatocyte Growth Factor and Vascular Endothelial Growth Factor in the Eyes with Angiogenic and Nonangiogenic Fibroproliferation

“…In PVR, the RPE cells proliferate and migrate as soon as the neural retina detaches from the RPE layer. These cells frequently lack pigment granules and exhibit a macrophage or fibroblast-like morphologic phenotype [35]. Recently, it was reported that RPE cell shape transformed to a more fibroblast-like appearance in the presence of HGF and c-Met in vitro [36].…”

Changes in Gene Expression of ARPE-19 Cells in Response to Vitreous Treatment

“…The in vitro vitreous model for investigating phenotypic changes and proliferative behavior of RPE cells has been widely used by many investigators [3,5,6,14]. Our study shows for the first time some of the changes in gene expression that are associated with the vitreous-induced phenotypic and proliferative alterations.…”

“…Vitreous treatment of cultured, subconfluent RPE cells leads to changes similar to that seen in PVR and provides a model for studying the pathological role of RPE in the development of this dis-ease [3][4][5][6]. After exposure to vitreous (in the presence of serum), RPE cells become proliferative and migratory and mimic the initial stages of wound healing, which is the hallmark of PVR in the eye [1,3,5,6]. In spite of numerous publications about the pathogenesis, the role of various cytokines and the source of epiretinal membranes in this disease, little information is known about the earliest molecular events that occur at the gene level during the onset of PVR.…”

“…As a result, among the genes that change their expression in response to vitreous, some encode for proteins found in the vitreous cavity or epiretinal membranes from patients with PVR, such as PDGF, ICAM-1, V-CAM1 and MCP-1 [15][16][17][18][19][20], and many are related to proliferative and migratory activity characteristic of a repair response. These findings provide additional evidence that vitreous stimulates RPE gene expression that may be related to the pathogenic phenotype of PVR [3][4][5].…”

Subretinal organization in stage 5 retinopathy of prematurity

“…Factors within the serum appear to cause RPE cell migration [2]. Once in the vitreous cavity, RPE cells react to vitreous components such as fibronectin [16], collagen [14], and fibrin [15] by transforming into fibroblast-like cells and forming pseudopods capable of grasping collagen. RPE cells, in turn, can form transforming growth factorbeta [10], which has been shown to stimulate proliferation of fibroblasts and mediate collagen and fibronectin release [6,13].…”

Non-Paralleled Increase of Hepatocyte Growth Factor and Vascular Endothelial Growth Factor in the Eyes with Angiogenic and Nonangiogenic Fibroproliferation

“…In PVR, the RPE cells proliferate and migrate as soon as the neural retina detaches from the RPE layer. These cells frequently lack pigment granules and exhibit a macrophage or fibroblast-like morphologic phenotype [35]. Recently, it was reported that RPE cell shape transformed to a more fibroblast-like appearance in the presence of HGF and c-Met in vitro [36].…”

Changes in Gene Expression of ARPE-19 Cells in Response to Vitreous Treatment

“…The in vitro vitreous model for investigating phenotypic changes and proliferative behavior of RPE cells has been widely used by many investigators [3,5,6,14]. Our study shows for the first time some of the changes in gene expression that are associated with the vitreous-induced phenotypic and proliferative alterations.…”

“…Vitreous treatment of cultured, subconfluent RPE cells leads to changes similar to that seen in PVR and provides a model for studying the pathological role of RPE in the development of this dis-ease [3][4][5][6]. After exposure to vitreous (in the presence of serum), RPE cells become proliferative and migratory and mimic the initial stages of wound healing, which is the hallmark of PVR in the eye [1,3,5,6]. In spite of numerous publications about the pathogenesis, the role of various cytokines and the source of epiretinal membranes in this disease, little information is known about the earliest molecular events that occur at the gene level during the onset of PVR.…”

“…As a result, among the genes that change their expression in response to vitreous, some encode for proteins found in the vitreous cavity or epiretinal membranes from patients with PVR, such as PDGF, ICAM-1, V-CAM1 and MCP-1 [15][16][17][18][19][20], and many are related to proliferative and migratory activity characteristic of a repair response. These findings provide additional evidence that vitreous stimulates RPE gene expression that may be related to the pathogenic phenotype of PVR [3][4][5].…”

Subretinal organization in stage 5 retinopathy of prematurity

“…Factors within the serum appear to cause RPE cell migration [2]. Once in the vitreous cavity, RPE cells react to vitreous components such as fibronectin [16], collagen [14], and fibrin [15] by transforming into fibroblast-like cells and forming pseudopods capable of grasping collagen. RPE cells, in turn, can form transforming growth factorbeta [10], which has been shown to stimulate proliferation of fibroblasts and mediate collagen and fibronectin release [6,13].…”

Non-Paralleled Increase of Hepatocyte Growth Factor and Vascular Endothelial Growth Factor in the Eyes with Angiogenic and Nonangiogenic Fibroproliferation

“…In PVR, the RPE cells proliferate and migrate as soon as the neural retina detaches from the RPE layer. These cells frequently lack pigment granules and exhibit a macrophage or fibroblast-like morphologic phenotype [35]. Recently, it was reported that RPE cell shape transformed to a more fibroblast-like appearance in the presence of HGF and c-Met in vitro [36].…”

Changes in Gene Expression of ARPE-19 Cells in Response to Vitreous Treatment

“…The in vitro vitreous model for investigating phenotypic changes and proliferative behavior of RPE cells has been widely used by many investigators [3,5,6,14]. Our study shows for the first time some of the changes in gene expression that are associated with the vitreous-induced phenotypic and proliferative alterations.…”

“…Vitreous treatment of cultured, subconfluent RPE cells leads to changes similar to that seen in PVR and provides a model for studying the pathological role of RPE in the development of this dis-ease [3][4][5][6]. After exposure to vitreous (in the presence of serum), RPE cells become proliferative and migratory and mimic the initial stages of wound healing, which is the hallmark of PVR in the eye [1,3,5,6]. In spite of numerous publications about the pathogenesis, the role of various cytokines and the source of epiretinal membranes in this disease, little information is known about the earliest molecular events that occur at the gene level during the onset of PVR.…”

“…As a result, among the genes that change their expression in response to vitreous, some encode for proteins found in the vitreous cavity or epiretinal membranes from patients with PVR, such as PDGF, ICAM-1, V-CAM1 and MCP-1 [15][16][17][18][19][20], and many are related to proliferative and migratory activity characteristic of a repair response. These findings provide additional evidence that vitreous stimulates RPE gene expression that may be related to the pathogenic phenotype of PVR [3][4][5].…”

Subretinal organization in stage 5 retinopathy of prematurity

“…Factors within the serum appear to cause RPE cell migration [2]. Once in the vitreous cavity, RPE cells react to vitreous components such as fibronectin [16], collagen [14], and fibrin [15] by transforming into fibroblast-like cells and forming pseudopods capable of grasping collagen. RPE cells, in turn, can form transforming growth factorbeta [10], which has been shown to stimulate proliferation of fibroblasts and mediate collagen and fibronectin release [6,13].…”