| First Author | Grimaldo S | Year | 2011 |
| Journal | Invest Ophthalmol Vis Sci | Volume | 52 |
| Issue | 7 | Pages | 4808-12 |
| PubMed ID | 21372020 | Mgi Jnum | J:181438 |
| Mgi Id | MGI:5311311 | Doi | 10.1167/iovs.10-6580 |
| Citation | Grimaldo S, et al. (2011) Very late antigen-1 mediates corneal lymphangiogenesis. Invest Ophthalmol Vis Sci 52(7):4808-12 |
| abstractText | PURPOSE: To investigate the specific role of very late antigen-1 (VLA-1; also known as integrin alpha1beta1) in corneal inflammatory lymphangiogenesis in vivo and lymphatic endothelial cell functions in vitro. METHODS: A standard suture-induced corneal inflammatory lymphangiogenesis model was used in normal adult BALB/c mice to test the effect of systemic administration of VLA-1-neutralizing antibody on lymphatic formation and macrophage infiltration in vivo. Additionally, a human lymphatic endothelial cell culture system was used to examine the effect of VLA-1 gene depletion on lymphatic endothelial cell functions in vitro using small interfering RNAs. RESULTS: These data demonstrated, for the first time, that VLA-1 blockade significantly suppressed corneal lymphangiogenesis and macrophage infiltration during inflammation. Moreover, VLA-1 gene depletion led to a marked inhibition of lymphatic endothelial cell processes of adhesion, proliferation, and capillary tube formation. CONCLUSIONS: These novel findings together indicate that VLA-1 is critically involved in the processes of lymphangiogenesis. Further investigation on this factor may provide novel therapies for corneal inflammation, transplant rejection, and other lymphatic-related disorders in the body. |
