The Experts below are selected from a list of 132 Experts worldwide ranked by ideXlab platform
Frank J Lovicu - One of the best experts on this subject based on the ideXlab platform.
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aqueous humour induced lens epithelial cell proliferation requires fgf signalling
Growth Factors Journal, 2017Co-Authors: L Iyengar, Frank J LovicuAbstract:AbstractThe eye lens grows by systematic proliferation of its epithelial cells and their differentiation into fibre cells. The anterior aqueous humour regulates lens epithelial cell proliferation whereas posteriorly, the vitreous stimulates lens fibre differentiation. Vitreous-derived members of the fibroblast growth factor (FGF) family induce fibre differentiation, with added support for FGFs as putative regulators of aqueous-induced lens cell proliferation. To further characterize this, given FGFs’ known affinity for proteoglycans, we compared the effect of proteoglycan sulphation in growth factor- and aqueous-induced lens cell proliferation. Disruption of proteoglycan sulphation in lens cells specifically impacted on aqueous- and FGF-induced MAPK/ERK1/2-signalling, but not on that induced by other Mitogens such as PDGF; however, cell proliferation was reduced in all treatment groups, regardless of the Mitogen. Overall, by disrupting proteoglycan activity, we further highlight the significant role of FG...
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aqueous humour and growth factor induced lens cell proliferation is dependent on mapk erk1 2 and akt pi3 k signalling
Experimental Eye Research, 2006Co-Authors: L Iyengar, Bramilla Patkunanathan, Oonagh T Lynch, John W Mcavoy, John E J Rasko, Frank J LovicuAbstract:The aqueous humour of the eye is a rich source of growth factors, many of which have been shown to be lens cell Mitogens; however, the identity of the endogenous Mitogen(s) for lens cells is still unknown. As a first approach to identify the mechanisms by which these aqueous humour-derived growth factors induce lens cell proliferation, the present study set out to examine MAPK/ERK1/2 and PI3-K/Akt signalling associated with lens cell proliferation. Using a lens explant system, we examined the effects of different lens Mitogens (aqueous humour, FGF, PDGF, IGF and EGF) using 5'-2'-bromo-deoxyuridine incorporation. In addition, we adopted immunolabelling techniques to compare the roles that the ERK1/2 and PI3-K signalling pathways play in regulating lens cell proliferation. We showed that the aqueous humour, and all the other growth factors examined, could activate ERK1/2 and PI3-K/Akt signalling. By targeting these pathways using specific pharmacological inhibitors, we were able to show that both ERK1/2 and PI3-K signalling are required for growth factor-induced lens cell proliferation, and that there was a strong correlation between the spatial distribution of proliferating cells in lens explants with ERK1/2 labelling. Furthermore, our blocking studies confirmed that PI3-K/Akt signalling can act upstream of ERK1/2, potentiating ERK1/2 phosphorylation in growth factor-induced lens cell proliferation. A better understanding of the signalling pathways required for aqueous humour-induced lens cell proliferation may ultimately allow us to identify the Mitogen(s) that are important for regulating lens cell proliferation in situ.
Richard I Weiner - One of the best experts on this subject based on the ideXlab platform.
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camp dependent protein kinase inhibits the Mitogenic action of vascular endothelial growth factor and fibroblast growth factor in capillary endothelial cells by blocking raf activation
Journal of Cellular Biochemistry, 1997Co-Authors: Gisela Dangelo, Richard I WeinerAbstract:Proliferation of endothelial cells is regulated by angiogenic and antiangiogenic factors whose actions are mediated by complex interactions of multiple signaling pathways. Both vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) stimulate cell proliferation and activate the Mitogen-activated protein kinase (MAPK) cascade in bovine brain capillary endothelial (BBE) cells. We have extended these findings to show that both Mitogens activate MAPK via stimulation of Raf-1. Activation of Raf/MAPK is inhibited by increasing intracellular cAMP levels pharmacologically or via stimulation of endogenously expressed β-adrenergic receptors. Both VEGF- and bFGF-induced Raf-1 activity are blocked in the presence of forskolin or 8-bromo-cAMP by 80%. The actions of increased cAMP appear to be mediated by cAMP-dependent protein kinase (PKA), since treatment with H-89, a the specific inhibitor of PKA, reversed the inhibitory effect of elevated cAMP levels on Mitogen-induced cell proliferation and Raf/MAPK activation. Moreover, elevations in cAMP/PKA activity inhibit Mitogen-induced cell proliferation. These findings demonstrate, in cultured endothelial cells, that the cAMP/PKA signaling pathway is potentially an important physiological inhibitor of Mitogen activation of the MAPK cascade and cell proliferation. J. Cell. Biochem. 67:353–366, 1997. © 1997 Wiley-Liss, Inc.
L Iyengar - One of the best experts on this subject based on the ideXlab platform.
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aqueous humour induced lens epithelial cell proliferation requires fgf signalling
Growth Factors Journal, 2017Co-Authors: L Iyengar, Frank J LovicuAbstract:AbstractThe eye lens grows by systematic proliferation of its epithelial cells and their differentiation into fibre cells. The anterior aqueous humour regulates lens epithelial cell proliferation whereas posteriorly, the vitreous stimulates lens fibre differentiation. Vitreous-derived members of the fibroblast growth factor (FGF) family induce fibre differentiation, with added support for FGFs as putative regulators of aqueous-induced lens cell proliferation. To further characterize this, given FGFs’ known affinity for proteoglycans, we compared the effect of proteoglycan sulphation in growth factor- and aqueous-induced lens cell proliferation. Disruption of proteoglycan sulphation in lens cells specifically impacted on aqueous- and FGF-induced MAPK/ERK1/2-signalling, but not on that induced by other Mitogens such as PDGF; however, cell proliferation was reduced in all treatment groups, regardless of the Mitogen. Overall, by disrupting proteoglycan activity, we further highlight the significant role of FG...
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aqueous humour and growth factor induced lens cell proliferation is dependent on mapk erk1 2 and akt pi3 k signalling
Experimental Eye Research, 2006Co-Authors: L Iyengar, Bramilla Patkunanathan, Oonagh T Lynch, John W Mcavoy, John E J Rasko, Frank J LovicuAbstract:The aqueous humour of the eye is a rich source of growth factors, many of which have been shown to be lens cell Mitogens; however, the identity of the endogenous Mitogen(s) for lens cells is still unknown. As a first approach to identify the mechanisms by which these aqueous humour-derived growth factors induce lens cell proliferation, the present study set out to examine MAPK/ERK1/2 and PI3-K/Akt signalling associated with lens cell proliferation. Using a lens explant system, we examined the effects of different lens Mitogens (aqueous humour, FGF, PDGF, IGF and EGF) using 5'-2'-bromo-deoxyuridine incorporation. In addition, we adopted immunolabelling techniques to compare the roles that the ERK1/2 and PI3-K signalling pathways play in regulating lens cell proliferation. We showed that the aqueous humour, and all the other growth factors examined, could activate ERK1/2 and PI3-K/Akt signalling. By targeting these pathways using specific pharmacological inhibitors, we were able to show that both ERK1/2 and PI3-K signalling are required for growth factor-induced lens cell proliferation, and that there was a strong correlation between the spatial distribution of proliferating cells in lens explants with ERK1/2 labelling. Furthermore, our blocking studies confirmed that PI3-K/Akt signalling can act upstream of ERK1/2, potentiating ERK1/2 phosphorylation in growth factor-induced lens cell proliferation. A better understanding of the signalling pathways required for aqueous humour-induced lens cell proliferation may ultimately allow us to identify the Mitogen(s) that are important for regulating lens cell proliferation in situ.
John W Mcavoy - One of the best experts on this subject based on the ideXlab platform.
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aqueous humour and growth factor induced lens cell proliferation is dependent on mapk erk1 2 and akt pi3 k signalling
Experimental Eye Research, 2006Co-Authors: L Iyengar, Bramilla Patkunanathan, Oonagh T Lynch, John W Mcavoy, John E J Rasko, Frank J LovicuAbstract:The aqueous humour of the eye is a rich source of growth factors, many of which have been shown to be lens cell Mitogens; however, the identity of the endogenous Mitogen(s) for lens cells is still unknown. As a first approach to identify the mechanisms by which these aqueous humour-derived growth factors induce lens cell proliferation, the present study set out to examine MAPK/ERK1/2 and PI3-K/Akt signalling associated with lens cell proliferation. Using a lens explant system, we examined the effects of different lens Mitogens (aqueous humour, FGF, PDGF, IGF and EGF) using 5'-2'-bromo-deoxyuridine incorporation. In addition, we adopted immunolabelling techniques to compare the roles that the ERK1/2 and PI3-K signalling pathways play in regulating lens cell proliferation. We showed that the aqueous humour, and all the other growth factors examined, could activate ERK1/2 and PI3-K/Akt signalling. By targeting these pathways using specific pharmacological inhibitors, we were able to show that both ERK1/2 and PI3-K signalling are required for growth factor-induced lens cell proliferation, and that there was a strong correlation between the spatial distribution of proliferating cells in lens explants with ERK1/2 labelling. Furthermore, our blocking studies confirmed that PI3-K/Akt signalling can act upstream of ERK1/2, potentiating ERK1/2 phosphorylation in growth factor-induced lens cell proliferation. A better understanding of the signalling pathways required for aqueous humour-induced lens cell proliferation may ultimately allow us to identify the Mitogen(s) that are important for regulating lens cell proliferation in situ.
Gisela Dangelo - One of the best experts on this subject based on the ideXlab platform.
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camp dependent protein kinase inhibits the Mitogenic action of vascular endothelial growth factor and fibroblast growth factor in capillary endothelial cells by blocking raf activation
Journal of Cellular Biochemistry, 1997Co-Authors: Gisela Dangelo, Richard I WeinerAbstract:Proliferation of endothelial cells is regulated by angiogenic and antiangiogenic factors whose actions are mediated by complex interactions of multiple signaling pathways. Both vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) stimulate cell proliferation and activate the Mitogen-activated protein kinase (MAPK) cascade in bovine brain capillary endothelial (BBE) cells. We have extended these findings to show that both Mitogens activate MAPK via stimulation of Raf-1. Activation of Raf/MAPK is inhibited by increasing intracellular cAMP levels pharmacologically or via stimulation of endogenously expressed β-adrenergic receptors. Both VEGF- and bFGF-induced Raf-1 activity are blocked in the presence of forskolin or 8-bromo-cAMP by 80%. The actions of increased cAMP appear to be mediated by cAMP-dependent protein kinase (PKA), since treatment with H-89, a the specific inhibitor of PKA, reversed the inhibitory effect of elevated cAMP levels on Mitogen-induced cell proliferation and Raf/MAPK activation. Moreover, elevations in cAMP/PKA activity inhibit Mitogen-induced cell proliferation. These findings demonstrate, in cultured endothelial cells, that the cAMP/PKA signaling pathway is potentially an important physiological inhibitor of Mitogen activation of the MAPK cascade and cell proliferation. J. Cell. Biochem. 67:353–366, 1997. © 1997 Wiley-Liss, Inc.
