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Glucocorticoids suppress corneal lymphangiogenesis
Maria M Steele1, Philip M Kelley, Amanda M Schieler
1Department of Genetics, Boys Town National Research Hospital, Omaha, NE 68131, USA.
Cornea
|September 30, 2011
Summary
Glucocorticoids, like dexamethasone, suppress new corneal lymphatic vessel growth (lymphangiogenesis) but do not cause existing vessels to regress. This reveals a new way glucocorticoids work in the eye.
Area of Science:
- Ophthalmology
- Immunology
- Cell Biology
Background:
- Glucocorticoids are potent anti-inflammatory drugs.
- Their effect on corneal lymphangiogenesis is not well understood.
- Understanding this mechanism is crucial for treating eye diseases.
Purpose of the Study:
- To investigate if glucocorticoids suppress corneal lymphatic vessel growth (lymphangiogenesis).
- To determine if glucocorticoids induce lymphatic vessel regression.
- To explore the mechanism of glucocorticoid action in the cornea.
Main Methods:
- Assessed human lymphatic endothelial cell proliferation and tubulogenesis in vitro with dexamethasone.
- Utilized a modified mouse corneal suture model to visualize lymphangiogenesis and regression.
- Quantified corneal lymphatic vessels and measured gene expression of VEGF-C and TNF-α.
Main Results:
- High-dose dexamethasone did not affect human lymphatic endothelial cell proliferation or tubulogenesis in vitro.
- Dexamethasone suppressed corneal lymphatic vessel growth, but did not induce regression in mice.
- Corneal VEGF-C and TNF-α mRNA expression remained unchanged by dexamethasone treatment.
Conclusions:
- Dexamethasone suppresses the formation of new corneal lymphatic vessels (lymphangiogenesis).
- Dexamethasone does not induce regression of existing corneal lymphatic vessels.
- This study identifies glucocorticoid-induced suppression of lymphangiogenesis as a novel mechanism.
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