国际眼科杂志
國際眼科雜誌
국제안과잡지
INTERNATIONAL JOURNAL OF OPHTHALMOLOGY
2014年
12期
2131-2134
,共4页
底煜%张轶欧%杨飏%陈晓隆
底煜%張軼歐%楊飏%陳曉隆
저욱%장질구%양양%진효륭
视网膜新生血管%富含半胱氨酸蛋白61%RNA干扰%早产儿视网膜病变
視網膜新生血管%富含半胱氨痠蛋白61%RNA榦擾%早產兒視網膜病變
시망막신생혈관%부함반광안산단백61%RNA간우%조산인시망막병변
retinal neovascularization%cysteine-rich 61%RNA interference%retinopathy of prematurity
目的：研究富含半胱氨酸蛋白61( CCN1/Cyr61)在氧诱导小鼠视网膜新生血管( retinal neovascularization, RNV)中的表达及意义,探讨特异性抑制CCN1对RNV形成的抑制作用。<br> 方法：取 C57 BL/6 J 小鼠200只,随机分为对照组、高氧组、高氧对照组和CCN1治疗组,每组各50只。高氧对照组和CCN1治疗组分别玻璃体腔内注射空载体质粒和CCN1 siRNA表达质粒。 ADP酶视网膜铺片观察视网膜血管形态,HE染色计数突破视网膜内界膜的新生血管内皮细胞核数,免疫组织化学、Western blot 和RT-PCR法检测CCN1蛋白及mRNA的表达情况。<br> 结果：高氧组和高氧对照组视网膜可见大片无灌注区和大量突破内界膜的新生血管内皮细胞核(25.25±1.26个；23.12±1.16个),CCN1治疗组较高氧组和高氧对照组的无灌注区及新生血管内皮细胞核数(8.47±1.15个)明显减少。高氧组和高氧对照组较对照组相比,CCN1蛋白及mRNA表达显著增高, CCN1治疗组较高氧组和高氧对照组显著减弱,均有统计学意义(均为P<0.05)。<br> 结论：CCN1的异常表达可能与RNV形成密切相关,特异性抑制 CCN1能有效抑制 RNV 的形成,为预防和治疗ROP提供新的思路及对策。
目的：研究富含半胱氨痠蛋白61( CCN1/Cyr61)在氧誘導小鼠視網膜新生血管( retinal neovascularization, RNV)中的錶達及意義,探討特異性抑製CCN1對RNV形成的抑製作用。<br> 方法：取 C57 BL/6 J 小鼠200隻,隨機分為對照組、高氧組、高氧對照組和CCN1治療組,每組各50隻。高氧對照組和CCN1治療組分彆玻璃體腔內註射空載體質粒和CCN1 siRNA錶達質粒。 ADP酶視網膜鋪片觀察視網膜血管形態,HE染色計數突破視網膜內界膜的新生血管內皮細胞覈數,免疫組織化學、Western blot 和RT-PCR法檢測CCN1蛋白及mRNA的錶達情況。<br> 結果：高氧組和高氧對照組視網膜可見大片無灌註區和大量突破內界膜的新生血管內皮細胞覈(25.25±1.26箇；23.12±1.16箇),CCN1治療組較高氧組和高氧對照組的無灌註區及新生血管內皮細胞覈數(8.47±1.15箇)明顯減少。高氧組和高氧對照組較對照組相比,CCN1蛋白及mRNA錶達顯著增高, CCN1治療組較高氧組和高氧對照組顯著減弱,均有統計學意義(均為P<0.05)。<br> 結論：CCN1的異常錶達可能與RNV形成密切相關,特異性抑製 CCN1能有效抑製 RNV 的形成,為預防和治療ROP提供新的思路及對策。
목적：연구부함반광안산단백61( CCN1/Cyr61)재양유도소서시망막신생혈관( retinal neovascularization, RNV)중적표체급의의,탐토특이성억제CCN1대RNV형성적억제작용。<br> 방법：취 C57 BL/6 J 소서200지,수궤분위대조조、고양조、고양대조조화CCN1치료조,매조각50지。고양대조조화CCN1치료조분별파리체강내주사공재체질립화CCN1 siRNA표체질립。 ADP매시망막포편관찰시망막혈관형태,HE염색계수돌파시망막내계막적신생혈관내피세포핵수,면역조직화학、Western blot 화RT-PCR법검측CCN1단백급mRNA적표체정황。<br> 결과：고양조화고양대조조시망막가견대편무관주구화대량돌파내계막적신생혈관내피세포핵(25.25±1.26개；23.12±1.16개),CCN1치료조교고양조화고양대조조적무관주구급신생혈관내피세포핵수(8.47±1.15개)명현감소。고양조화고양대조조교대조조상비,CCN1단백급mRNA표체현저증고, CCN1치료조교고양조화고양대조조현저감약,균유통계학의의(균위P<0.05)。<br> 결론：CCN1적이상표체가능여RNV형성밀절상관,특이성억제 CCN1능유효억제 RNV 적형성,위예방화치료ROP제공신적사로급대책。
AlM: 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. <br> 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. <br> 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). <br> CONCLUSlON: 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.
