角膜上皮 MT1-MMP 抑制血管内皮细胞的增殖和迁移。
Corneal epithelial MT1-MMP inhibits vascular endothelial cell proliferation and migration.
机构信息
Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, IL, USA.
出版信息
Cornea. 2010 Mar;29(3):321-30. doi: 10.1097/ICO.0b013e3181b1165d.
Abstract
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'-deoxy-uridine (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.
摘要
目的
确定角膜上皮膜型 1 基质金属蛋白酶（MT1-MMP）对血管内皮细胞迁移和增殖的影响。
方法
我们生成了永生化的野生型、MT1-MMP 敲除和 MT1-MMP 敲入角膜上皮细胞。检测牛肺动脉内皮（CPAE）细胞的增殖和 Boyden 室迁移。
结果
与野生型上皮细胞相比，MT1-MMP 上皮敲除细胞的条件培养基显著增加了 CPAE 增殖（5-溴-2'-脱氧尿苷（BrdU）掺入）和 CPAE 迁移。来自敲入细胞的条件培养基逆转了 CPAE 增殖、BrdU 掺入和 CPAE 迁移的增加。转染突变型 MT1-MMP（E240A）的敲入细胞不会消除逆转作用。
结论
角膜上皮 MT1-MMP 具有抗血管生成作用。这种抗血管生成活性不需要催化结构域。
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