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

Cited 0 time in webofscience Cited 28 time in scopus
Kim, Jeong Hun; Kim, Ki Hyun; Kim, Jin Hyoung; Yu, Young Suk; Kim, Young-Myeong; Kim, Kyu-Won; Kwon, Ho Jeong
Issue Date
Academic Press
Biochem Biophys Res Commun. 2007 Nov 3;362(4):848-52. Epub 2007 Aug 28.
AnimalsCDC2 Protein Kinase/*metabolismCell Cycle/drug effectsDisease Models, AnimalDose-Response Relationship, DrugDown-Regulation/drug effectsHumansInfant, NewbornIsoflavones/*therapeutic useMiceMice, Inbred C57BLRetinal Neovascularization/*drug therapy/*metabolism/pathologyRetinopathy of Prematurity/*drug therapy/*metabolism/pathology
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 microM. 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.
0006-291X (Print)
Files in This Item:
There are no files associated with this item.
Appears in Collections:
College of Medicine/School of Medicine (의과대학/대학원)Ophthalmology (안과학전공)Journal Papers (저널논문_안과학전공)
  • mendeley

Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.