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Published on: April 7, 2014
Inhibition of corneal neovascularization by rapamycin
1Department of Ophthalmology, Chung-Ang University, Yongsan Hospital, College of Medicine, Seoul 140-757, Korea.
Abstract:
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.
Insights
Rapamycin effectively inhibits corneal angiogenesis triggered by basic fibroblast growth factor (bFGF). This study demonstrates rapamycin
Area of Science:
- Ophthalmology
- Pharmacology
- Cell Biology
Background:
- Corneal angiogenesis, the formation of new blood vessels in the cornea, can impair vision.
- Basic fibroblast growth factor (bFGF) is a known inducer of angiogenesis.
- Identifying effective anti-angiogenic agents is crucial for treating vision-threatening corneal conditions.
Purpose of the Study:
- To investigate the inhibitory effect of rapamycin on basic fibroblast growth factor (bFGF)-induced corneal angiogenesis.
- To evaluate rapamycin's impact on endothelial cell behavior and vascular endothelial growth factor (VEGF) expression in vitro.
- To assess the therapeutic potential of rapamycin as an anti-angiogenic agent in a corneal model.
Main Methods:
- In vitro studies using human dermal microvascular endothelial cells (HDMECs) to assess proliferation, migration, and VEGF secretion.
- In vivo experiments involving intrastromal corneal implantation of bFGF with or without rapamycin in a rabbit micropocket model.
- Biomicrographic and histological evaluation of corneal neovascularization over 10 days.
Main Results:
- Rapamycin significantly inhibited bFGF-induced proliferation, migration, and VEGF secretion in HDMECs.
- In the rabbit corneal micropocket model, rapamycin treatment markedly reduced bFGF-induced corneal neovascularization.
- Histological analysis confirmed a significant decrease in new blood vessel formation in the rapamycin-treated group compared to controls.
Conclusions:
- Rapamycin demonstrates potent anti-angiogenic properties against bFGF-induced corneal neovascularization.
- The findings suggest rapamycin's potential as a therapeutic agent for ocular conditions characterized by excessive blood vessel growth.
- Further research into rapamycin's clinical application for corneal angiogenesis is warranted.
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