The Experts below are selected from a list of 4389 Experts worldwide ranked by ideXlab platform
Careen Y. Lowder - One of the best experts on this subject based on the ideXlab platform.
-
PERIPHERAL RETINOSCHISIS IN INTERMEDIATE UVEITIS.
Retina (Philadelphia Pa.), 2017Co-Authors: Francesco Pichi, Sunil K. Srivastava, Paolo Nucci, Kimberly Baynes, Piergiorgio Neri, Careen Y. LowderAbstract:PURPOSE To examine cases of intermediate uveitis complicated by retinoschisis and review the pathogenetic hypothesis. METHODS A retrospective chart review of patients with intermediate uveitis. Data were collected at three uveitis referral centers on sex, age, best-corrected visual acuity, degree of vitritis, extent and location of snowbanking, presence of hard exudates, Neovascularization, vitreous hemorrhage, and extent and nature of Retinal elevations. RESULTS A series of 23 eyes of 20 patients were examined; patient's age ranged from 10 years to 70 years and follow-up period from 8 months to 6 years. Twenty-two eyes had retinoschisis (95.6%), and 1 had retinoschisis associated with serous Retinal detachment (4.3%). Extensive inferior pars plana exudates with snowbanking were present in 12 eyes (52.2%), whereas 3 eyes had inferior snowballs over the elevated Retina. Neovascularization of the vitreous base accompanied by vitreous hemorrhage occurred in one eye. There was no coexisting macular pathology in 16 eyes, whereas 4 eyes had cystoid macular edema. CONCLUSION The appearance of peripheral retinoschisis in this series of uncontrolled intermediate uveitis patients seems to be secondary to a complex balance between the persistent fluorescein leakage, a subclinical peripheral ischemia, and the constant low-grade vitreous inflammation that causes vitreous shrinkage and traction. The results of this study suggest that the absence of macroscopic changes in the Retina does not preclude ischemic peripheral abnormalities, and the detection of a peripheral retinoschisis in an intermediate uveitis patient with active fluorescein leakage must suggest the need for a more aggressive form of treatment despite the good visual acuity.
Li Xiaoxin - One of the best experts on this subject based on the ideXlab platform.
-
Semaphorin 3A blocks the formation of pathologic choroidal Neovascularization induced by transforming growth factor beta
molecular vision, 2014Co-Authors: Bai Yujing, Liang Shuting, Yu Wenzhen, Zhao Min, Huang Lvzhen, Zhao Mingwei, Li XiaoxinAbstract:Objective: Choroidal Neovascularization (CNV) is a major cause of vision loss in Retinal diseases such as age-related macular degeneration (AMD). Previously, we demonstrated that semaphorin3A (Sema3A), which is a chemorepellent guidance molecule, inhibited the formation of Retina Neovascularization. In the present study, we investigated the anti-angiogenic effects of Sema3A on transforming growth factor beta (TGF-beta) in vitro and in vivo. Methods: Enzyme-linked immunosorbent assays (ELISAs) were used to measure the TGF-beta levels in the vitreous humor of patients with AMD and controls. Human umbilical vein endothelial cells (HUVECs) were used for the in vitro study, and a laser-induced CNV mouse model was prepared for the in vivo study. The HUVECs were incubated with TGF-beta and Sema3A. The proliferation, migration, apoptosis, and tube formation of the cells were then measured using BrdU, Transwell, flow cytometry, and Matrigel assays, respectively, and the SMAD2/3 signaling pathways were analyzed using western blot analysis. The C57BL/6J mouse Retina was exposed to a laser to induce choroidal Neovascularization (CNV), and Sema3A was injected intravitreously. After 14 days, fundus fluorescein angiography was performed to evaluate the leakage area of the CNV. The vascular endothelial growth factor (VEGF) and TGF-beta concentrations in the Retina-choroid complex were measured with ELISA. Components of the p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase-1/2 (ERK1/2), c-Jun NH2-terminal kinase (JNK), and SMAD2/3 signaling pathways in the Sema3A-treated groups were analyzed using western blotting. Results: In this study, we first verified that the vitreous TGF-beta level was higher in patients with neovascular AMD than in the controls. We also showed that Sema3A inhibited TGF-beta-induced HUVEC proliferation, migration, and tube formation and inhibited the downstream SMAD2/3 signaling pathway. Sema3A also induced TGF-beta-stimulated HUVEC apoptosis and inhibited the response of TGF-beta in vitro. In vivo, the TGF-beta level was increased in the CNV mouse model. Sema3A not only inhibited laser-induced CNV formation but also inhibited the uptake of VEGF and TGF-beta. In the western blot analysis, Sema3A was shown to inhibit the phosphorylation of p38 MAPK, ERK1/2, and JNK and to inhibit the SMAD2/3 signaling pathway after Sema3A treatment in CNV mice. Conclusions: Sema3A can be applied as a useful, adjunctive therapeutic strategy for preventing CNV formation.http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000341976900001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701Biochemistry & Molecular BiologyOphthalmologySCI(E)PubMed6ARTICLE41379226@qq.com1258-12702
Francesco Pichi - One of the best experts on this subject based on the ideXlab platform.
-
PERIPHERAL RETINOSCHISIS IN INTERMEDIATE UVEITIS.
Retina (Philadelphia Pa.), 2017Co-Authors: Francesco Pichi, Sunil K. Srivastava, Paolo Nucci, Kimberly Baynes, Piergiorgio Neri, Careen Y. LowderAbstract:PURPOSE To examine cases of intermediate uveitis complicated by retinoschisis and review the pathogenetic hypothesis. METHODS A retrospective chart review of patients with intermediate uveitis. Data were collected at three uveitis referral centers on sex, age, best-corrected visual acuity, degree of vitritis, extent and location of snowbanking, presence of hard exudates, Neovascularization, vitreous hemorrhage, and extent and nature of Retinal elevations. RESULTS A series of 23 eyes of 20 patients were examined; patient's age ranged from 10 years to 70 years and follow-up period from 8 months to 6 years. Twenty-two eyes had retinoschisis (95.6%), and 1 had retinoschisis associated with serous Retinal detachment (4.3%). Extensive inferior pars plana exudates with snowbanking were present in 12 eyes (52.2%), whereas 3 eyes had inferior snowballs over the elevated Retina. Neovascularization of the vitreous base accompanied by vitreous hemorrhage occurred in one eye. There was no coexisting macular pathology in 16 eyes, whereas 4 eyes had cystoid macular edema. CONCLUSION The appearance of peripheral retinoschisis in this series of uncontrolled intermediate uveitis patients seems to be secondary to a complex balance between the persistent fluorescein leakage, a subclinical peripheral ischemia, and the constant low-grade vitreous inflammation that causes vitreous shrinkage and traction. The results of this study suggest that the absence of macroscopic changes in the Retina does not preclude ischemic peripheral abnormalities, and the detection of a peripheral retinoschisis in an intermediate uveitis patient with active fluorescein leakage must suggest the need for a more aggressive form of treatment despite the good visual acuity.
Bai Yujing - One of the best experts on this subject based on the ideXlab platform.
-
Semaphorin 3A blocks the formation of pathologic choroidal Neovascularization induced by transforming growth factor beta
molecular vision, 2014Co-Authors: Bai Yujing, Liang Shuting, Yu Wenzhen, Zhao Min, Huang Lvzhen, Zhao Mingwei, Li XiaoxinAbstract:Objective: Choroidal Neovascularization (CNV) is a major cause of vision loss in Retinal diseases such as age-related macular degeneration (AMD). Previously, we demonstrated that semaphorin3A (Sema3A), which is a chemorepellent guidance molecule, inhibited the formation of Retina Neovascularization. In the present study, we investigated the anti-angiogenic effects of Sema3A on transforming growth factor beta (TGF-beta) in vitro and in vivo. Methods: Enzyme-linked immunosorbent assays (ELISAs) were used to measure the TGF-beta levels in the vitreous humor of patients with AMD and controls. Human umbilical vein endothelial cells (HUVECs) were used for the in vitro study, and a laser-induced CNV mouse model was prepared for the in vivo study. The HUVECs were incubated with TGF-beta and Sema3A. The proliferation, migration, apoptosis, and tube formation of the cells were then measured using BrdU, Transwell, flow cytometry, and Matrigel assays, respectively, and the SMAD2/3 signaling pathways were analyzed using western blot analysis. The C57BL/6J mouse Retina was exposed to a laser to induce choroidal Neovascularization (CNV), and Sema3A was injected intravitreously. After 14 days, fundus fluorescein angiography was performed to evaluate the leakage area of the CNV. The vascular endothelial growth factor (VEGF) and TGF-beta concentrations in the Retina-choroid complex were measured with ELISA. Components of the p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase-1/2 (ERK1/2), c-Jun NH2-terminal kinase (JNK), and SMAD2/3 signaling pathways in the Sema3A-treated groups were analyzed using western blotting. Results: In this study, we first verified that the vitreous TGF-beta level was higher in patients with neovascular AMD than in the controls. We also showed that Sema3A inhibited TGF-beta-induced HUVEC proliferation, migration, and tube formation and inhibited the downstream SMAD2/3 signaling pathway. Sema3A also induced TGF-beta-stimulated HUVEC apoptosis and inhibited the response of TGF-beta in vitro. In vivo, the TGF-beta level was increased in the CNV mouse model. Sema3A not only inhibited laser-induced CNV formation but also inhibited the uptake of VEGF and TGF-beta. In the western blot analysis, Sema3A was shown to inhibit the phosphorylation of p38 MAPK, ERK1/2, and JNK and to inhibit the SMAD2/3 signaling pathway after Sema3A treatment in CNV mice. Conclusions: Sema3A can be applied as a useful, adjunctive therapeutic strategy for preventing CNV formation.http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000341976900001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701Biochemistry & Molecular BiologyOphthalmologySCI(E)PubMed6ARTICLE41379226@qq.com1258-12702
Sunil K. Srivastava - One of the best experts on this subject based on the ideXlab platform.
-
PERIPHERAL RETINOSCHISIS IN INTERMEDIATE UVEITIS.
Retina (Philadelphia Pa.), 2017Co-Authors: Francesco Pichi, Sunil K. Srivastava, Paolo Nucci, Kimberly Baynes, Piergiorgio Neri, Careen Y. LowderAbstract:PURPOSE To examine cases of intermediate uveitis complicated by retinoschisis and review the pathogenetic hypothesis. METHODS A retrospective chart review of patients with intermediate uveitis. Data were collected at three uveitis referral centers on sex, age, best-corrected visual acuity, degree of vitritis, extent and location of snowbanking, presence of hard exudates, Neovascularization, vitreous hemorrhage, and extent and nature of Retinal elevations. RESULTS A series of 23 eyes of 20 patients were examined; patient's age ranged from 10 years to 70 years and follow-up period from 8 months to 6 years. Twenty-two eyes had retinoschisis (95.6%), and 1 had retinoschisis associated with serous Retinal detachment (4.3%). Extensive inferior pars plana exudates with snowbanking were present in 12 eyes (52.2%), whereas 3 eyes had inferior snowballs over the elevated Retina. Neovascularization of the vitreous base accompanied by vitreous hemorrhage occurred in one eye. There was no coexisting macular pathology in 16 eyes, whereas 4 eyes had cystoid macular edema. CONCLUSION The appearance of peripheral retinoschisis in this series of uncontrolled intermediate uveitis patients seems to be secondary to a complex balance between the persistent fluorescein leakage, a subclinical peripheral ischemia, and the constant low-grade vitreous inflammation that causes vitreous shrinkage and traction. The results of this study suggest that the absence of macroscopic changes in the Retina does not preclude ischemic peripheral abnormalities, and the detection of a peripheral retinoschisis in an intermediate uveitis patient with active fluorescein leakage must suggest the need for a more aggressive form of treatment despite the good visual acuity.