Corneal Epithelial MT1-MMP Inhibits Vascular Endothelial Cell Proliferation and Migration

被引:13
作者
Azar, Dimitri T. [1 ,2 ,3 ]
Casanova, Fabio H. [2 ,3 ]
Mimura, Tatsuya [1 ,2 ]
Jain, Sandeep [1 ,3 ]
Zhou, Zhongjun [4 ]
Han, Kyu Yeon [1 ]
Chang, Jin-Hong [1 ,2 ,3 ]
机构
[1] Univ Illinois, Dept Ophthalmol & Visual Sci, Chicago, IL 60612 USA
[2] Harvard Univ, Sch Med, Schepens Eye Res Inst, Boston, MA USA
[3] Massachusetts Eye & Ear Infirm, Dept Ophthalmol, Boston, MA 02114 USA
[4] Univ Hong Kong, Dept Biochem, Hong Kong, Hong Kong, Peoples R China
基金
美国国家卫生研究院;
关键词
cornea; MT1-MMP; TIMP; epithelium; TYPE-1; MATRIX-METALLOPROTEINASE; IN-VITRO; TISSUE INHIBITOR; ANGIOGENESIS; SURFACE; VEGF; NEOVASCULARIZATION; OLIGOMERIZATION; AVASCULARITY; PROTEOLYSIS;
D O I
10.1097/ICO.0b013e3181b1165d
中图分类号
R77 [眼科学];
学科分类号
100212 [眼科学];
摘要
Purpose: To determine the effects of corneal epithelial membrane-type 1 matrix metalloproteinase (MT1-MMP) on vascular endothelial migration and proliferation. Methods: We generated immortalized wild-type, MT1-MMP knockout and MT1-MMP knock-in corneal epithelial cells. Calf pulmonary arterial endothelial (CPAE) cell proliferation and Boyden chamber migration were assayed. Results: Conditioned media from MT1-MMP epithelial knockout cells significantly increased CPAE proliferation 5-bromo-2'-deoxyuridine (BrdU) incorporation, and CPAE migration as compared with wild-type epithelial cells. Conditioned media from knock-in cells reversed the increase in CPAE proliferation, BrdU incorporation and CPAE migration. Knock-in cells transfected with mutant MT1-MMP (E240A) did not abrogate the reversal effect. Conclusions: Corneal epithelial MT1-MMP is antiangiogenic. This antiangiogenic activity does not require the catalytic domain.
引用
收藏
页码:321 / 330
页数:10
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