Effect of bradykinin on TGF-β1-induced retinal pigment epithelial cell proliferation and extracellular matrix secretion

被引:7
作者
Cai, Wenting [1 ]
Wei, Qingquan [2 ]
Liu, Qingyu [1 ]
Ren, Chengda [1 ]
Liu, Junling [1 ]
Zhang, Ruiling [1 ]
He, Mengmei [1 ]
Wang, Qianyi [1 ]
Du, Yaru [3 ]
Yu, Jing [1 ]
机构
[1] Tongji Univ, Shanghai Peoples Hosp 10, Sch Med, Dept Ophthalmol, Shanghai, Peoples R China
[2] Nanchang Univ, Nanchang, Jiangxi, Peoples R China
[3] 180th Hosp Chinese Peoples Liberat Army, Dept Ophthalmol, Quanzhou, Fujian Province, Peoples R China
基金
中国国家自然科学基金;
关键词
Proliferative vitreoretinopathy; Retinal pigment epithelium; Bradykinin; Transforming growth factor-beta 1; Extracellular matrix; TGF-BETA; SUBRETINAL MEMBRANES; METALLOPROTEINASES; DETACHMENT; TGF-BETA-2; EXPRESSION; PROTEINS; DISEASE; FLUID;
D O I
10.1186/s12886-016-0373-3
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
Background: To evaluate the effect of bradykinin (BK) on TGF-beta 1-induced retinal pigment epithelial (RPE) cell proliferation and extracellular matrix secretion and to elucidate the relationship between BK and the Erk/Akt signaling pathway. Methods: The effects of BK on TGF-beta 1-induced RPE cell proliferation were examined via CCK-8 assay. Cell culture supernatant collagen I concentrations were measured via ELISA. Fibronectin (Fn), matrix metalloproteinase-2 (MMP-2) and MMP-9 mRNA and protein expression levels were measured via q-PCR and Western blotting, respectively. Changes in Akt/Erk phosphorylation induced by BK and HOE-140 were evaluated via Western blotting. Results: TGF-beta 1 stimulated ARPE-19 cell proliferation, which was inhibited by BK, whose effects were inhibited by HOE-140. BK inhibited TGF-beta 1-induced collagen I, Fn and MMP-2 secretion in RPE cells, and these effects were inhibited by HOE-140. BK also inhibited TGF-beta 1-induced Akt phosphorylation in RPE cells, and these effects were blocked by HOE-140. BK had no significant effect on Erk-mediated signaling. Conclusions: The findings from this study indicate that BK could be novel therapeutic targets for the treatment of PVR.
引用
收藏
页码:1 / 9
页数:9
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