Homoisoflavanone inhibits retinal neovascularization through cell cycle arrest with decrease of cdc2 expression

Jeong Hun Kim; Ki Hyun Kim; Jin Hyoung Kim; Young Suk Yu; Young Myeong Kim; Kyu Won Kim; Ho Jeong Kwon

doi:10.1016/j.bbrc.2007.08.100

Homoisoflavanone inhibits retinal neovascularization through cell cycle arrest with decrease of cdc2 expression

Jeong Hun Kim, Ki Hyun Kim, Jin Hyoung Kim, Young Suk Yu, Young Myeong Kim, Kyu Won Kim, Ho Jeong Kwon

Research output: Contribution to journal › Article › peer-review

38 Citations (Scopus)

Abstract

Neovascularization in the eye is the most common cause of blindness in all age groups; retinopathy of prematurity (ROP), diabetic retinopathy, and age-related macular degeneration. Despite current advances in surgical treatments, ROP remains as the most serious problem of vision loss in children. Here, we report that homoisoflavanone, a natural product from Cremastra appendiculata, significantly reduces retinal neovascularization in a mouse model of ROP. Homoisoflavanone inhibited the cell growth of HUVECs, but its cytotoxic effect was not observed in a concentration range of 1-20 μM. HUVECs population gradually increased in G₂/M phase and reduced in G₀/G₁ and S phases after exposure to the compound. Homoisoflavanone decreased the level of cdc2 expression whereas the level of p21^WAF1 expression was increased in a dose-dependent manner. These data demonstrate that homoisoflavanone could inhibit retinal neovascularization and be applied in the treatment of other vasoproliferative retinopathies.

Original language	English
Pages (from-to)	848-852
Number of pages	5
Journal	Biochemical and Biophysical Research Communications
Volume	362
Issue number	4
DOIs	https://doi.org/10.1016/j.bbrc.2007.08.100
Publication status	Published - 2007 Nov 3

Bibliographical note

Funding Information:
We are grateful to Mr. Chang Sik Cho for the technical assistance of animal experiments. This study was supported by grants from the Bio-signal Analysis Technology Innovation Program (M1064501001-06n4501-00110) of the Ministry of Science and Technology (MOST), Korea Science and Engineering Foundation (KOSEF), Seoul R&BD Program (10541), and from the Brain Korea 21 Project, Republic of Korea.

All Science Journal Classification (ASJC) codes

Biophysics
Biochemistry
Molecular Biology
Cell Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.bbrc.2007.08.100

Cite this

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title = "Homoisoflavanone inhibits retinal neovascularization through cell cycle arrest with decrease of cdc2 expression",

abstract = "Neovascularization in the eye is the most common cause of blindness in all age groups; retinopathy of prematurity (ROP), diabetic retinopathy, and age-related macular degeneration. Despite current advances in surgical treatments, ROP remains as the most serious problem of vision loss in children. Here, we report that homoisoflavanone, a natural product from Cremastra appendiculata, significantly reduces retinal neovascularization in a mouse model of ROP. Homoisoflavanone inhibited the cell growth of HUVECs, but its cytotoxic effect was not observed in a concentration range of 1-20 μM. HUVECs population gradually increased in G2/M phase and reduced in G0/G1 and S phases after exposure to the compound. Homoisoflavanone decreased the level of cdc2 expression whereas the level of p21WAF1 expression was increased in a dose-dependent manner. These data demonstrate that homoisoflavanone could inhibit retinal neovascularization and be applied in the treatment of other vasoproliferative retinopathies.",

author = "Kim, {Jeong Hun} and Kim, {Ki Hyun} and Kim, {Jin Hyoung} and Yu, {Young Suk} and Kim, {Young Myeong} and Kim, {Kyu Won} and Kwon, {Ho Jeong}",

note = "Funding Information: We are grateful to Mr. Chang Sik Cho for the technical assistance of animal experiments. This study was supported by grants from the Bio-signal Analysis Technology Innovation Program (M1064501001-06n4501-00110) of the Ministry of Science and Technology (MOST), Korea Science and Engineering Foundation (KOSEF), Seoul R&BD Program (10541), and from the Brain Korea 21 Project, Republic of Korea.",

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AU - Yu, Young Suk

AU - Kim, Young Myeong

AU - Kim, Kyu Won

AU - Kwon, Ho Jeong

N1 - Funding Information: We are grateful to Mr. Chang Sik Cho for the technical assistance of animal experiments. This study was supported by grants from the Bio-signal Analysis Technology Innovation Program (M1064501001-06n4501-00110) of the Ministry of Science and Technology (MOST), Korea Science and Engineering Foundation (KOSEF), Seoul R&BD Program (10541), and from the Brain Korea 21 Project, Republic of Korea.

PY - 2007/11/3

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N2 - Neovascularization in the eye is the most common cause of blindness in all age groups; retinopathy of prematurity (ROP), diabetic retinopathy, and age-related macular degeneration. Despite current advances in surgical treatments, ROP remains as the most serious problem of vision loss in children. Here, we report that homoisoflavanone, a natural product from Cremastra appendiculata, significantly reduces retinal neovascularization in a mouse model of ROP. Homoisoflavanone inhibited the cell growth of HUVECs, but its cytotoxic effect was not observed in a concentration range of 1-20 μM. HUVECs population gradually increased in G2/M phase and reduced in G0/G1 and S phases after exposure to the compound. Homoisoflavanone decreased the level of cdc2 expression whereas the level of p21WAF1 expression was increased in a dose-dependent manner. These data demonstrate that homoisoflavanone could inhibit retinal neovascularization and be applied in the treatment of other vasoproliferative retinopathies.

AB - Neovascularization in the eye is the most common cause of blindness in all age groups; retinopathy of prematurity (ROP), diabetic retinopathy, and age-related macular degeneration. Despite current advances in surgical treatments, ROP remains as the most serious problem of vision loss in children. Here, we report that homoisoflavanone, a natural product from Cremastra appendiculata, significantly reduces retinal neovascularization in a mouse model of ROP. Homoisoflavanone inhibited the cell growth of HUVECs, but its cytotoxic effect was not observed in a concentration range of 1-20 μM. HUVECs population gradually increased in G2/M phase and reduced in G0/G1 and S phases after exposure to the compound. Homoisoflavanone decreased the level of cdc2 expression whereas the level of p21WAF1 expression was increased in a dose-dependent manner. These data demonstrate that homoisoflavanone could inhibit retinal neovascularization and be applied in the treatment of other vasoproliferative retinopathies.

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Homoisoflavanone inhibits retinal neovascularization through cell cycle arrest with decrease of cdc2 expression

Abstract

Bibliographical note

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