AIM: To explore the expression and significance of cysteine-rich 61(CCN1/Cyr61)in oxygen-induced retinal neovascularization(RNV)of mice and study the inhibition effect of CCN1 specific siRNA on RNV.

METHODS: Two hundred healthy C57BL/6J mice were chosen and randomly divided into control group, hyperxia group, hyperxia control group and CCN1 treated group, with 50 mice in each group. The hyperxia control group was treated with vector plasmids by intravitreal injection. The CCN1 treated group received CCN1 siRNA recombinant plasmids by intravitreal injection. Adenosine diphosphate-ase(ADPase)stained retina flat-mounts was performed to assess the retinal vascular profiles, HE staining was applied to count the number of vascular endothelial cell nuclei breaking through the internal limiting membrane, protein and mRNA level expression of CCN1 were measured by immunohistochemistry, Western blot and RT-PCR.

RESULTS: There were large nonperfusion area and a large number of vascular endothelial cell nuclei breaking through the internal limiting membrane(25.25±1.26; 23.12±1.16)in the hyperxia group and the hyperxia control group. Regions of nonperfusion and vascular endothelial cell nuclei(8.47±1.15)were decreased in the CCN1 treated group compared to the hyperxia group and the hyperxia control group. Compared with the control group, there were high protein and mRNA expression of CCN1 in the hyperxia group and the hyperxia control group. The expression of CCN1 protein and mRNA were decreased in the CCN1 treated group compared with the hyperxia group and hyperxia control group(all P<0.05).

CONCLUSION: The abnormal expression of CCN1 has close relation with RNV. The development of RNV can be markedly inhibited by RNA interference targeting CCN1, which, we believe, will provide new molecular targets and a rationale for clinical developing new strategy for ROP therapy.