Pigment epithelium-derived factor acts as an opponent of growth-stimulatory factors in retinal glial-endothelial cell interactions
Pigment epithelium‐derived factor (PEDF), a glycoprotein with pleiotropic functions, is naturally occuring in the eye and considered as crucial to prevent pathological angiogenesis. Since retinal glial (Müller) cells produce PEDF, the authors have studied its impact on glial–endothelial cellular int...
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Published in | Glia Vol. 55; no. 6; pp. 642 - 651 |
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Abstract | Pigment epithelium‐derived factor (PEDF), a glycoprotein with pleiotropic functions, is naturally occuring in the eye and considered as crucial to prevent pathological angiogenesis. Since retinal glial (Müller) cells produce PEDF, the authors have studied its impact on glial–endothelial cellular interactions. Bovine retinal endothelial cells were cultured in the presence of culture media originating from primary Müller cells, and endothelial proliferation as well as phosphorylation of the mitogen‐activated protein kinases extracellular signal‐regulated kinases (ERK)‐1/‐2 were investigated. The concerted activity of Müller‐cell derived soluble mediators attenuated endothelial proliferation and ERK‐1/‐2 activation, regardless of whether the Müller cells were preincubated under normoxia or hypoxia, and even though the endothelial cells were stimulated by vascular endothelial growth factor‐A (VEGF). This inhibitory activity was no longer demonstrable if high levels of basic fibroblast growth factor or VEGF were supplied, suggesting that in cases of pathological neovascularization, overproduction of proangiogenic mediators overrides the “antiangiogenic background” provided by Müller cells. However, neutralizing the activity of PEDF partially restored endothelial cell proliferation and resulted in increased ERK‐1/‐2 activation, which is in concordance with findings demonstrating that exogenously applied PEDF is able to suppress VEGF‐induced ERK‐1/‐2 phosphorylation. PEDF production by Müller cells is not only regulated by retinal oxygen but also by the activity of soluble factors released from retinal endothelial cells. For instance, PEDF levels were significantly elevated in glial (Müller)–endothelial cell cocultures as compared with bovine retinal endothelial cell‐free Müller cell cultures. These results have implications for the pathogenesis of retinal neovascularization since the Müller cell may be regarded as a central control element which modulates retinal PEDF levels and, thus, is of critical importance for adjusting the balance between proangiogenic and antiangiogenic mediators. © 2007 Wiley‐Liss, Inc. |
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AbstractList | Pigment epithelium‐derived factor (PEDF), a glycoprotein with pleiotropic functions, is naturally occuring in the eye and considered as crucial to prevent pathological angiogenesis. Since retinal glial (Müller) cells produce PEDF, the authors have studied its impact on glial–endothelial cellular interactions. Bovine retinal endothelial cells were cultured in the presence of culture media originating from primary Müller cells, and endothelial proliferation as well as phosphorylation of the mitogen‐activated protein kinases extracellular signal‐regulated kinases (ERK)‐1/‐2 were investigated. The concerted activity of Müller‐cell derived soluble mediators attenuated endothelial proliferation and ERK‐1/‐2 activation, regardless of whether the Müller cells were preincubated under normoxia or hypoxia, and even though the endothelial cells were stimulated by vascular endothelial growth factor‐A (VEGF). This inhibitory activity was no longer demonstrable if high levels of basic fibroblast growth factor or VEGF were supplied, suggesting that in cases of pathological neovascularization, overproduction of proangiogenic mediators overrides the “antiangiogenic background” provided by Müller cells. However, neutralizing the activity of PEDF partially restored endothelial cell proliferation and resulted in increased ERK‐1/‐2 activation, which is in concordance with findings demonstrating that exogenously applied PEDF is able to suppress VEGF‐induced ERK‐1/‐2 phosphorylation. PEDF production by Müller cells is not only regulated by retinal oxygen but also by the activity of soluble factors released from retinal endothelial cells. For instance, PEDF levels were significantly elevated in glial (Müller)–endothelial cell cocultures as compared with bovine retinal endothelial cell‐free Müller cell cultures. These results have implications for the pathogenesis of retinal neovascularization since the Müller cell may be regarded as a central control element which modulates retinal PEDF levels and, thus, is of critical importance for adjusting the balance between proangiogenic and antiangiogenic mediators. © 2007 Wiley‐Liss, Inc. Pigment epithelium-derived factor (PEDF), a glycoprotein with pleiotropic functions, is naturally occuring in the eye and considered as crucial to prevent pathological angiogenesis. Since retinal glial (Muller) cells produce PEDF, the authors have studied its impact on glial-endothelial cellular interactions. Bovine retinal endothelial cells were cultured in the presence of culture media originating from primary Muller cells, and endothelial proliferation as well as phosphorylation of the mitogen-activated protein kinases extracellular signal-regulated kinases (ERK)-1/-2 were investigated. The concerted activity of Muller-cell derived soluble mediators attenuated endothelial proliferation and ERK-1/-2 activation, regardless of whether the Muller cells were preincubated under normoxia or hypoxia, and even though the endothelial cells were stimulated by vascular endothelial growth factor-A (VEGF). This inhibitory activity was no longer demonstrable if high levels of basic fibroblast growth factor or VEGF were supplied, suggesting that in cases of pathological neovascularization, overproduction of proangiogenic mediators overrides the antiangiogenic background provided by Muller cells. However, neutralizing the activity of PEDF partially restored endothelial cell proliferation and resulted in increased ERK-1/-2 activation, which is in concordance with findings demonstrating that exogenously applied PEDF is able to suppress VEGF-induced ERK-1/-2 phosphorylation. PEDF production by Muller cells is not only regulated by retinal oxygen but also by the activity of soluble factors released from retinal endothelial cells. For instance, PEDF levels were significantly elevated in glial (Muller)-endothelial cell cocultures as compared with bovine retinal endothelial cell-free Muller cell cultures. These results have implications for the pathogenesis of retinal neovascularization since the Muller cell may be regarded as a central control element which modulates retinal PEDF levels and, thus, is of critical importance for adjusting the balance between proangiogenic and antiangiogenic mediators. Abstract Pigment epithelium‐derived factor (PEDF), a glycoprotein with pleiotropic functions, is naturally occuring in the eye and considered as crucial to prevent pathological angiogenesis. Since retinal glial (Müller) cells produce PEDF, the authors have studied its impact on glial–endothelial cellular interactions. Bovine retinal endothelial cells were cultured in the presence of culture media originating from primary Müller cells, and endothelial proliferation as well as phosphorylation of the mitogen‐activated protein kinases extracellular signal‐regulated kinases (ERK)‐1/‐2 were investigated. The concerted activity of Müller‐cell derived soluble mediators attenuated endothelial proliferation and ERK‐1/‐2 activation, regardless of whether the Müller cells were preincubated under normoxia or hypoxia, and even though the endothelial cells were stimulated by vascular endothelial growth factor‐A (VEGF). This inhibitory activity was no longer demonstrable if high levels of basic fibroblast growth factor or VEGF were supplied, suggesting that in cases of pathological neovascularization, overproduction of proangiogenic mediators overrides the “antiangiogenic background” provided by Müller cells. However, neutralizing the activity of PEDF partially restored endothelial cell proliferation and resulted in increased ERK‐1/‐2 activation, which is in concordance with findings demonstrating that exogenously applied PEDF is able to suppress VEGF‐induced ERK‐1/‐2 phosphorylation. PEDF production by Müller cells is not only regulated by retinal oxygen but also by the activity of soluble factors released from retinal endothelial cells. For instance, PEDF levels were significantly elevated in glial (Müller)–endothelial cell cocultures as compared with bovine retinal endothelial cell‐free Müller cell cultures. These results have implications for the pathogenesis of retinal neovascularization since the Müller cell may be regarded as a central control element which modulates retinal PEDF levels and, thus, is of critical importance for adjusting the balance between proangiogenic and antiangiogenic mediators. © 2007 Wiley‐Liss, Inc. Pigment epithelium-derived factor (PEDF), a glycoprotein with pleiotropic functions, is naturally occuring in the eye and considered as crucial to prevent pathological angiogenesis. Since retinal glial (Müller) cells produce PEDF, the authors have studied its impact on glial-endothelial cellular interactions. Bovine retinal endothelial cells were cultured in the presence of culture media originating from primary Müller cells, and endothelial proliferation as well as phosphorylation of the mitogen-activated protein kinases extracellular signal-regulated kinases (ERK)-1/-2 were investigated. The concerted activity of Müller-cell derived soluble mediators attenuated endothelial proliferation and ERK-1/-2 activation, regardless of whether the Müller cells were preincubated under normoxia or hypoxia, and even though the endothelial cells were stimulated by vascular endothelial growth factor-A (VEGF). This inhibitory activity was no longer demonstrable if high levels of basic fibroblast growth factor or VEGF were supplied, suggesting that in cases of pathological neovascularization, overproduction of proangiogenic mediators overrides the "antiangiogenic background" provided by Müller cells. However, neutralizing the activity of PEDF partially restored endothelial cell proliferation and resulted in increased ERK-1/-2 activation, which is in concordance with findings demonstrating that exogenously applied PEDF is able to suppress VEGF-induced ERK-1/-2 phosphorylation. PEDF production by Müller cells is not only regulated by retinal oxygen but also by the activity of soluble factors released from retinal endothelial cells. For instance, PEDF levels were significantly elevated in glial (Müller)-endothelial cell cocultures as compared with bovine retinal endothelial cell-free Müller cell cultures. These results have implications for the pathogenesis of retinal neovascularization since the Müller cell may be regarded as a central control element which modulates retinal PEDF levels and, thus, is of critical importance for adjusting the balance between proangiogenic and antiangiogenic mediators. |
Author | Yafai, Yousef Eichler, Wolfram Reichenbach, Andreas Wiedemann, Peter Lange, Johannes |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/17309061$$D View this record in MEDLINE/PubMed |
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Snippet | Pigment epithelium‐derived factor (PEDF), a glycoprotein with pleiotropic functions, is naturally occuring in the eye and considered as crucial to prevent... Pigment epithelium-derived factor (PEDF), a glycoprotein with pleiotropic functions, is naturally occuring in the eye and considered as crucial to prevent... Abstract Pigment epithelium‐derived factor (PEDF), a glycoprotein with pleiotropic functions, is naturally occuring in the eye and considered as crucial to... |
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SubjectTerms | angiogenesis Animals Cattle Cell Communication - physiology Cell Proliferation - drug effects Cells, Cultured Coculture Techniques cytokine Endothelial Cells - cytology Endothelial Cells - metabolism Enzyme Activation - drug effects Enzyme Activation - physiology Extracellular Signal-Regulated MAP Kinases - drug effects Extracellular Signal-Regulated MAP Kinases - metabolism Eye Proteins - metabolism Eye Proteins - pharmacology Growth Inhibitors - metabolism Growth Inhibitors - pharmacology Guinea Pigs Intercellular Signaling Peptides and Proteins - metabolism Intercellular Signaling Peptides and Proteins - secretion MAP Kinase Signaling System - drug effects MAP Kinase Signaling System - physiology Müller cell Neovascularization, Pathologic - metabolism Neovascularization, Pathologic - physiopathology Nerve Growth Factors - metabolism Nerve Growth Factors - pharmacology Neuroglia - cytology Neuroglia - metabolism Oxygen Consumption - drug effects Oxygen Consumption - physiology PEDF Pigment Epithelium of Eye - cytology Pigment Epithelium of Eye - metabolism Pigment Epithelium of Eye - secretion proliferation retina Retina - cytology Retina - metabolism Retinal Artery - cytology Retinal Artery - drug effects Retinal Artery - metabolism Serpins - metabolism Serpins - pharmacology Vascular Endothelial Growth Factor A - antagonists & inhibitors Vascular Endothelial Growth Factor A - metabolism Vascular Endothelial Growth Factor A - secretion |
Title | Pigment epithelium-derived factor acts as an opponent of growth-stimulatory factors in retinal glial-endothelial cell interactions |
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