PURPOSE: To analyze the role of VEGF and its receptors, VEGFR2/Flk1 and VEGFR1/Flt1, on retinal progenitor cells (RPCs) in a murine model of inherited retinal degeneration (rd1 mice). METHODS: After proliferating RPCs in the retina of rd1 mice were labeled with bromodeoxyuridine (BrdU), expressions of VEGFR2/Flk1 and VEGFR1/Flt1 were immunohistochemically analyzed. To examine its effect on the proliferation of BrdU-positive RPCs in rd1 mice, VEGF was administered into retinal culture medium with or without blocking agents against VEGFR2/Flk1 or VEGFR1/Flt1 in vitro or injected into vitreous cavity in vivo. RESULTS: BrdU-labeled RPCs in rd1 mice expressed VEGFR2/Flk1 but not VEGFR1/Flt1. These cells later expressed retinal neuronal markers such as Pax6 and rhodopsin. Exposure of the retinas from postnatal day (P) 9 rd1 mice to VEGF increased the number of proliferating RPCs by 61% in vitro. This effect was blocked by concomitant administration of VEGFR2/Flk1 kinase inhibitor. In vivo, a single intravitreal injection of VEGF in rd1 mice at P9 increased by 138% the number of RPCs and cells that developed from RPCs in the peripheral retina at P18. CONCLUSIONS: VEGF stimulates the proliferation of RPCs through VEGFR2/Flk1 in rd1 mice. The observed proliferation of RPCs that have the potential to differentiate into retinal neurons may enhance the regeneration of the degenerating retina.
PURPOSE: To analyze the role of VEGF and its receptors, VEGFR2/Flk1 and VEGFR1/Flt1, on retinal progenitor cells (RPCs) in a murine model of inherited retinal degeneration (rd1mice). METHODS: After proliferating RPCs in the retina of rd1mice were labeled with bromodeoxyuridine (BrdU), expressions of VEGFR2/Flk1 and VEGFR1/Flt1 were immunohistochemically analyzed. To examine its effect on the proliferation of BrdU-positive RPCs in rd1mice, VEGF was administered into retinal culture medium with or without blocking agents against VEGFR2/Flk1 or VEGFR1/Flt1 in vitro or injected into vitreous cavity in vivo. RESULTS:BrdU-labeled RPCs in rd1mice expressed VEGFR2/Flk1 but not VEGFR1/Flt1. These cells later expressed retinal neuronal markers such as Pax6 and rhodopsin. Exposure of the retinas from postnatal day (P) 9 rd1mice to VEGF increased the number of proliferating RPCs by 61% in vitro. This effect was blocked by concomitant administration of VEGFR2/Flk1 kinase inhibitor. In vivo, a single intravitreal injection of VEGF in rd1mice at P9 increased by 138% the number of RPCs and cells that developed from RPCs in the peripheral retina at P18. CONCLUSIONS:VEGF stimulates the proliferation of RPCs through VEGFR2/Flk1 in rd1mice. The observed proliferation of RPCs that have the potential to differentiate into retinal neurons may enhance the regeneration of the degenerating retina.
Authors: Marco Adán Juárez-Verdayes; Sandra Rodríguez-Martínez; Mario E Cancino-Diaz; Juan C Cancino-Diaz Journal: Graefes Arch Clin Exp Ophthalmol Date: 2012-08-14 Impact factor: 3.117
Authors: Anne B Fulton; James D Akula; Julie A Mocko; Ronald M Hansen; Ilan Y Benador; Susanne C Beck; Edda Fahl; Mathias W Seeliger; Anne Moskowitz; Maureen E Harris Journal: Doc Ophthalmol Date: 2008-05-16 Impact factor: 2.379
Authors: Laura E Schultz; Staci L Solin; Wesley A Wierson; Janna M Lovan; Judith Syrkin-Nikolau; Deborah E Lincow; Andrew J Severin; Donald S Sakaguchi; Maura McGrail Journal: Zebrafish Date: 2017-02-13 Impact factor: 1.985