 | Related Articles |
?A-crystallin in the pathogenesis and intervention of experimental murine corneal neovascularization.
Exp Eye Res. 2012 May;98:44-51
Authors: Zhu W, Qi X, Ren S, Jia C, Song Z, Wang Y
Abstract
This study was to determine the potential roles of lens crystallins in the pathogenesis of corneal neovascularization (CorNV) and implications in therapy of CorNV-related diseases. Suture- or chemical burn-induced CorNV in different strains of mice were used. Changes of gene expression patterns were analyzed by microarray, and the results of interesting genes were confirmed by real-time quantitative PCR and Western blot. Mice deficient in ?A-crystallin gene were used to evaluate the role of ?A-crystallin in the development of CorNV. In some animals, exogenous ?A-crystallin proteins were injected around time of CorNV induction. CorNV was assessed by slit-lamp, flat-mounts and histology. In BALB/C mice, the expression of ?-, ?-, and ?-crystallins were up-regulated at day 5 and returned to baseline level at day 10 of suture-induced CorNV, but remained up-regulated from day 6 to day 14 of chemical burn-induced CorNV. In chemical burn-induced CorNV in C57BL/6J mice, however, they were down-regulated at day 6. Corneal crystallins were down-regulated in both CorNV models at all time points in both BALB/c and C57BL/6J mice. Comparison of CorNV development in ?A-crystallin-deficient mice and that in wild-type mice revealed no significant difference. Subconjunctival injection of ?A-crystallin significantly attenuated suture-induced CorNV, and the inhibitory activity might be implemented by the increased expression of�soluble VEGFR-1. In conclusion, the expression patterns of lens crystallins were time- and strain-dependent but different from that of corneal crystallins in mouse CorNV models. Exogenous ?A-crystallin protein attenuated CorNV, potentially by increasing the expression of soluble VEGFR-1.
PMID: 22465406 [PubMed - indexed for MEDLINE]
没有评论:
发表评论