Inhibition of choroidal neovascularization by homoisoflavanone, a new angiogenesis inhibitor

Jeong Hun Kim, Jin Hyoung Kim, Young Suk Yu, Hyoung Oh Jun, Ho Jeong Kwon, Kyu Hyung Park, Kyu Won Kim

Research output: Contribution to journalArticle

22 Citations (Scopus)

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-y1)-2,5-diphentyltetrazolium bromide assay (MTT) assay in HUVECs as weli 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 μM. 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.

Original languageEnglish
Pages (from-to)556-561
Number of pages6
JournalMolecular Vision
Volume14
Publication statusPublished - 2008 Mar 18

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Choroidal Neovascularization
Angiogenesis Inhibitors
Human Umbilical Vein Endothelial Cells
Light Coagulation
Macular Degeneration
Lasers
Cell Migration Assays
DNA Nucleotidylexotransferase
Fluorescein Angiography
Blindness
Biotin
Inhibition (Psychology)
Bromides
Cell Movement
Retina
Cell Survival
Staining and Labeling

All Science Journal Classification (ASJC) codes

  • Ophthalmology

Cite this

Kim, J. H., Kim, J. H., Yu, Y. S., Jun, H. O., Kwon, H. J., Park, K. H., & Kim, K. W. (2008). Inhibition of choroidal neovascularization by homoisoflavanone, a new angiogenesis inhibitor. Molecular Vision, 14, 556-561.
Kim, Jeong Hun ; Kim, Jin Hyoung ; Yu, Young Suk ; Jun, Hyoung Oh ; Kwon, Ho Jeong ; Park, Kyu Hyung ; Kim, Kyu Won. / Inhibition of choroidal neovascularization by homoisoflavanone, a new angiogenesis inhibitor. In: Molecular Vision. 2008 ; Vol. 14. pp. 556-561.
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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-y1)-2,5-diphentyltetrazolium bromide assay (MTT) assay in HUVECs as weli 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 μM. 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.",
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Kim, JH, Kim, JH, Yu, YS, Jun, HO, Kwon, HJ, Park, KH & Kim, KW 2008, 'Inhibition of choroidal neovascularization by homoisoflavanone, a new angiogenesis inhibitor', Molecular Vision, vol. 14, pp. 556-561.

Inhibition of choroidal neovascularization by homoisoflavanone, a new angiogenesis inhibitor. / Kim, Jeong Hun; Kim, Jin Hyoung; Yu, Young Suk; Jun, Hyoung Oh; Kwon, Ho Jeong; Park, Kyu Hyung; Kim, Kyu Won.

In: Molecular Vision, Vol. 14, 18.03.2008, p. 556-561.

Research output: Contribution to journalArticle

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T1 - Inhibition of choroidal neovascularization by homoisoflavanone, a new angiogenesis inhibitor

AU - Kim, Jeong Hun

AU - Kim, Jin Hyoung

AU - Yu, Young Suk

AU - Jun, Hyoung Oh

AU - Kwon, Ho Jeong

AU - Park, Kyu Hyung

AU - Kim, Kyu Won

PY - 2008/3/18

Y1 - 2008/3/18

N2 - 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-y1)-2,5-diphentyltetrazolium bromide assay (MTT) assay in HUVECs as weli 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 μM. 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.

AB - 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-y1)-2,5-diphentyltetrazolium bromide assay (MTT) assay in HUVECs as weli 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 μM. 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.

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