Limits...
Inhibition of choroidal neovascularization by homoisoflavanone, a new angiogenesis inhibitor.

Kim JH, Kim JH, Yu YS, Jun HO, Kwon HJ, Park KH, Kim KW - Mol. Vis. (2008)

Bottom Line: Homoisoflavanone effectively inhibited in vitro tube formation and cell migration of HUVECs.Interestingly, homoisoflavanone significantly reduced CNV and its leakage in a mouse model of laser-photocoagulation-induced CNV.In addition, homoisoflavanone showed no effect on cell viability of HUVECs and no retinal toxicity in a concentration range of 1-10 microM.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, College of Medicine, Seoul National University, Seoul Artificial Eye Center Clinical ResearchInstitute, Seoul National University Hospital, Seoul, Korea.

ABSTRACT

Purpose: Age-related macular degeneration (AMD) is the leading cause of blindness in elderly. The detailed mechanism of choroidal neovascularization (CNV) leads to severe vision loss in patients with AMD. This study was undertaken to evaluate the inhibitory effect of homoisoflavanone on CNV.

Methods: Antiangiogenic activity of homoisoflavanone was evaluated by in vitro tube formation assay of human umbilical vein endothelial cells (HUVECs) and cell migration assay of HUVECs., Homoisoflavanone or PBS was injected intravitreously into a mouse model of laser-photocoagulation-induced CNV. Fluorescein angiography and vessel counting in cross sections were employed to examine CNV lesions. The toxicity of homoisoflavanone was evaluated through 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay (MTT) assay in HUVECs as well as histological examination and terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) staining in the retina.

Results: Homoisoflavanone effectively inhibited in vitro tube formation and cell migration of HUVECs. Interestingly, homoisoflavanone significantly reduced CNV and its leakage in a mouse model of laser-photocoagulation-induced CNV. In addition, homoisoflavanone showed no effect on cell viability of HUVECs and no retinal toxicity in a concentration range of 1-10 microM.

Conclusions: Our data suggest that homoisoflavanone is a potent inhibitor of CNV and may be applied in the treatment of other vasoproliferative retinopathies and tumor.

Show MeSH

Related in: MedlinePlus

Effect of homoisoflavanone on fibroblast growth factor-2 and human umbilical vein endothelial cells. A: Each figure is representative of three independent experiments. B: Basal tube formation of human umbilical vein endothelial cells (HUVECs) left in serum-free media was normalized to 100% respectively. Each value represents means ± SEM from three independent experiments (*p<0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC2274926&req=5

f1: Effect of homoisoflavanone on fibroblast growth factor-2 and human umbilical vein endothelial cells. A: Each figure is representative of three independent experiments. B: Basal tube formation of human umbilical vein endothelial cells (HUVECs) left in serum-free media was normalized to 100% respectively. Each value represents means ± SEM from three independent experiments (*p<0.05).

Mentions: To investigate the effect of homoisoflavanone on an angiogenic phenotype of tube formation in vitro assay, we used FGF-2 as an angiogenic factor. FGF-2 induced the formation of extensive capillary-like networks of HUVECs cultured on two-dimensional Matrigel matrix. This effect was almost completely inhibited by co-treatment with homoisoflavanone (Figure 1A). FGF-2 stimulated tube formation of HUVECs approximately 1.4-fold, and this effect was abolished by homoisoflavanone (Figure 1B).


Inhibition of choroidal neovascularization by homoisoflavanone, a new angiogenesis inhibitor.

Kim JH, Kim JH, Yu YS, Jun HO, Kwon HJ, Park KH, Kim KW - Mol. Vis. (2008)

Effect of homoisoflavanone on fibroblast growth factor-2 and human umbilical vein endothelial cells. A: Each figure is representative of three independent experiments. B: Basal tube formation of human umbilical vein endothelial cells (HUVECs) left in serum-free media was normalized to 100% respectively. Each value represents means ± SEM from three independent experiments (*p<0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2274926&req=5

f1: Effect of homoisoflavanone on fibroblast growth factor-2 and human umbilical vein endothelial cells. A: Each figure is representative of three independent experiments. B: Basal tube formation of human umbilical vein endothelial cells (HUVECs) left in serum-free media was normalized to 100% respectively. Each value represents means ± SEM from three independent experiments (*p<0.05).
Mentions: To investigate the effect of homoisoflavanone on an angiogenic phenotype of tube formation in vitro assay, we used FGF-2 as an angiogenic factor. FGF-2 induced the formation of extensive capillary-like networks of HUVECs cultured on two-dimensional Matrigel matrix. This effect was almost completely inhibited by co-treatment with homoisoflavanone (Figure 1A). FGF-2 stimulated tube formation of HUVECs approximately 1.4-fold, and this effect was abolished by homoisoflavanone (Figure 1B).

Bottom Line: Homoisoflavanone effectively inhibited in vitro tube formation and cell migration of HUVECs.Interestingly, homoisoflavanone significantly reduced CNV and its leakage in a mouse model of laser-photocoagulation-induced CNV.In addition, homoisoflavanone showed no effect on cell viability of HUVECs and no retinal toxicity in a concentration range of 1-10 microM.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, College of Medicine, Seoul National University, Seoul Artificial Eye Center Clinical ResearchInstitute, Seoul National University Hospital, Seoul, Korea.

ABSTRACT

Purpose: Age-related macular degeneration (AMD) is the leading cause of blindness in elderly. The detailed mechanism of choroidal neovascularization (CNV) leads to severe vision loss in patients with AMD. This study was undertaken to evaluate the inhibitory effect of homoisoflavanone on CNV.

Methods: Antiangiogenic activity of homoisoflavanone was evaluated by in vitro tube formation assay of human umbilical vein endothelial cells (HUVECs) and cell migration assay of HUVECs., Homoisoflavanone or PBS was injected intravitreously into a mouse model of laser-photocoagulation-induced CNV. Fluorescein angiography and vessel counting in cross sections were employed to examine CNV lesions. The toxicity of homoisoflavanone was evaluated through 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay (MTT) assay in HUVECs as well as histological examination and terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) staining in the retina.

Results: Homoisoflavanone effectively inhibited in vitro tube formation and cell migration of HUVECs. Interestingly, homoisoflavanone significantly reduced CNV and its leakage in a mouse model of laser-photocoagulation-induced CNV. In addition, homoisoflavanone showed no effect on cell viability of HUVECs and no retinal toxicity in a concentration range of 1-10 microM.

Conclusions: Our data suggest that homoisoflavanone is a potent inhibitor of CNV and may be applied in the treatment of other vasoproliferative retinopathies and tumor.

Show MeSH
Related in: MedlinePlus