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Kwon YS, Kim JC
Exp Mol Med. 2006 Apr 30;38(2):173-9
Inhibition of corneal neovascularization by rapamycin.
Department of Ophthalmology, Chung-Ang University, Yongsan
Hospital, College of Medicine, Seoul 140-757, Korea.
The purpose of this study was to determine whether rapamycin could inhibit
corneal angiogenesis induced by basic fibroblast growth factor (bFGF). Using
human dermal microvascular endothelial cells (HDMECs), we examined the effect of
rapamycin on cell proliferation and migration, and the expression of vascular
endothelial growth factor (VEGF). The rabbit's eye was implanted intrastromally
into the superior cornea with pellet containing bFGF for the control group and
pellet containing bFGF and rapamycin for the rapamycin group.
Biomicrographically, corneal angiogenesis was evaluated for 10 days after pellet
implantation. The neovascularized cornea also was examined histologically. bFGF
induced corneal neovascularization was significantly reduced by treatment with
rapamycin. Using in vitro model, rapamycin strongly inhibited bFGF induced
proliferation, migration, and VEGF secretion of HDMECs. We could observe that
the bFGF induced corneal angiogenesis was inhibited by rapamycin in a
micropocket rabbit model. The score of neovascularization was significantly
decreased in the rapamycin group than in the control group at 10 days after
pellet implantation. Histologically, the cornea of rapamycin group also showed
much less new vessels than that of control group. Collectively, rapamycin
appears to inhibit bFGF induced angiogenesis in a rabbit corneal micropocket
assay and may have therapeutic potential as an antiangiogenic agent.
PMID: 16672771 |
