e-3330 and Retinal-Neovascularization

e-3330 has been researched along with Retinal-Neovascularization* in 1 studies

Other Studies

1 other study(ies) available for e-3330 and Retinal-Neovascularization

Article	Year
Inhibition of APE1/Ref-1 redox activity with APX3330 blocks retinal angiogenesis in vitro and in vivo. Vision research, 2011, Volume: 51, Issue:1 This study examines the role of APE1/Ref-1 in the retina and its potential as a therapeutic target for inhibiting retinal angiogenesis. APE1/Ref-1 expression was quantified by Western blot. The role of APE1/Ref-1 redox function in endothelial cell in vitro angiogenesis was examined by treating retinal vascular endothelial cells (RVECs) with APX3330, a small molecule inhibitor of APE1/Ref-1 redox activity. In vitro methods included a proliferation assay, a transwell migration assay, a Matrigel tube formation assay, and a Real-Time Cell Analysis (RTCA) using the xCELLigence System. In vivo functional studies of APE1/Ref-1 were carried out by treating very low density lipoprotein (VLDL) receptor knockout mice (Vldlr(-/-)) with intravitreal injection of APX3330, and subsequent measurement of retinal angiomatous proliferation (RAP)-like neovascularization for one week. APE1/Ref-1 was highly expressed in the retina and in RVECs and pericytes in mice. APX3330 (1-10 μM) inhibited proliferation, migration and tube formation of RVECs in vitro in a dose-dependent manner. Vldlr(-/-) RVECs were more sensitive to APX3330 than wild-type RVECs. In Vldlr(-/-) mice, a single intravitreal injection of APX3330 at the onset of RAP-like neovascularization significantly reduced RAP-like neovascularization development. APE1/Ref-1 is expressed in retinal vascular cells. APX3330 inhibits RVEC angiogenesis in vitro and significantly reduces RAP-like neovascularization in Vldlr(-/-) mice. These data support the conclusion that APE1/Ref-1 redox function is required for retinal angiogenesis. Thus, APE1/Ref-1 may have potential as a therapeutic target for treating neovascular age-related macular degeneration and other neovascular diseases. Topics: Animals; Apoptosis; Benzoquinones; Blotting, Western; Cell Movement; Cell Proliferation; Cells, Cultured; DNA-(Apurinic or Apyrimidinic Site) Lyase; Endothelium, Vascular; Mice; Mice, Knockout; Neovascularization, Pathologic; Oxidation-Reduction; Propionates; Retina; Retinal Neovascularization	2011

Article

Year

Inhibition of APE1/Ref-1 redox activity with APX3330 blocks retinal angiogenesis in vitro and in vivo.

Vision research, 2011, Volume: 51, Issue:1

This study examines the role of APE1/Ref-1 in the retina and its potential as a therapeutic target for inhibiting retinal angiogenesis. APE1/Ref-1 expression was quantified by Western blot. The role of APE1/Ref-1 redox function in endothelial cell in vitro angiogenesis was examined by treating retinal vascular endothelial cells (RVECs) with APX3330, a small molecule inhibitor of APE1/Ref-1 redox activity. In vitro methods included a proliferation assay, a transwell migration assay, a Matrigel tube formation assay, and a Real-Time Cell Analysis (RTCA) using the xCELLigence System. In vivo functional studies of APE1/Ref-1 were carried out by treating very low density lipoprotein (VLDL) receptor knockout mice (Vldlr(-/-)) with intravitreal injection of APX3330, and subsequent measurement of retinal angiomatous proliferation (RAP)-like neovascularization for one week. APE1/Ref-1 was highly expressed in the retina and in RVECs and pericytes in mice. APX3330 (1-10 μM) inhibited proliferation, migration and tube formation of RVECs in vitro in a dose-dependent manner. Vldlr(-/-) RVECs were more sensitive to APX3330 than wild-type RVECs. In Vldlr(-/-) mice, a single intravitreal injection of APX3330 at the onset of RAP-like neovascularization significantly reduced RAP-like neovascularization development. APE1/Ref-1 is expressed in retinal vascular cells. APX3330 inhibits RVEC angiogenesis in vitro and significantly reduces RAP-like neovascularization in Vldlr(-/-) mice. These data support the conclusion that APE1/Ref-1 redox function is required for retinal angiogenesis. Thus, APE1/Ref-1 may have potential as a therapeutic target for treating neovascular age-related macular degeneration and other neovascular diseases.

Topics: Animals; Apoptosis; Benzoquinones; Blotting, Western; Cell Movement; Cell Proliferation; Cells, Cultured; DNA-(Apurinic or Apyrimidinic Site) Lyase; Endothelium, Vascular; Mice; Mice, Knockout; Neovascularization, Pathologic; Oxidation-Reduction; Propionates; Retina; Retinal Neovascularization

2011