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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.
Purpose:
To determine whether glucocorticoids suppress corneal lymphatic vessel growth (lymphangiogenesis) or induce lymphatic vessel regression.
Methods:
We measured human lymphatic endothelial cell proliferation and collagen-induced tubulogenesis in culture conditions with and without dexamethasone, a potent glucocorticoid. We developed a modification of the mouse corneal suture model that allowed us to visualize lymphatic vessel growth (with suture) or regression (suture removed) using immunofluorescence and microscopic techniques. We administered dexamethasone or vehicle control to mice with sutured corneas. We visualized and quantified the corneal lymphatic vessels. We measured vascular endothelial growth factor-C and tumor necrosis factor-α messenger RNA expression in unsutured or sutured corneas using quantitative reverse transcriptase-polymerase chain reaction.
Results:
High-dose dexamethasone did not change the proliferation or tubulogenesis properties of human lymphatic endothelial cells in vitro. We demonstrated suppressed corneal lymphatic vessel growth rather than lymphatic vessel regression in mice treated with dexamethasone. Expressions of corneal vascular endothelial growth factor-C and tumor necrosis factor-α messenger RNA were similar in mice treated with or without dexamethasone.
Conclusions:
Dexamethasone suppressed new lymphatic vessel growth and did not induce lymphatic vessel regression. These findings identify a novel mechanism of glucocorticoid action: suppression of corneal lymphangiogenesis.
Insights
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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