Caspase-1 Plays a Critical Role in Accelerating Chronic Kidney Disease-Promoted Neointimal Hyperplasia in the Carotid Artery

被引：51

作者：

Ferrer, Lucas M. ^{[1
,2
]}

Monroy, Alexandra M. ^{[1
,2
]}

Lopez-Pastrana, Jahaira ^{[1
,2
]}

Nanayakkara, Gayani ^{[1
,2
]}

Cueto, Ramon ^{[1
,2
]}

Li, Ya-feng ^{[1
,2
]}

Li, Xinyuan ^{[1
,2
]}

Wang, Hong ^{[1
,2
,3
]}

Yang, Xiao-feng ^{[1
,2
,3
]}

Choi, Eric T. ^{[1
,2
,4
]}

机构：

[1] Temple Univ, Lewis Katz Sch Med, Ctr Metab Dis Res, 3500 North Broad St, Philadelphia, PA 19140 USA

[2] Temple Univ, Lewis Katz Sch Med, Ctr Cardiovasc Res & Thrombosis Res, 3500 North Broad St, Philadelphia, PA 19140 USA

[3] Temple Univ, Lewis Katz Sch Med, Dept Pharmacol, Philadelphia, PA 19140 USA

[4] Temple Univ, Lewis Katz Sch Med, Dept Surg, Philadelphia, PA 19140 USA

来源：

JOURNAL OF CARDIOVASCULAR TRANSLATIONAL RESEARCH | 2016年 / 9卷 / 02期

基金：

美国国家卫生研究院;

关键词：

Caspase-1; Vascular inflammation; Chronic kidney disease (CKD); Neointimal hyperplasia (NH); Vascular smooth muscle cell (VSMC); MUSCLE-CELL DIFFERENTIATION; VASCULAR INJURY; ATHEROSCLEROTIC LESIONS; DIALYSIS ACCESS; DEFICIENT MICE; INFLAMMASOMES; INFLAMMATION; ACTIVATION; CLASSIFICATION; EXPRESSION;

D O I：

10.1007/s12265-016-9683-3

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

To determine whether caspase-1 is critical in chronic kidney disease (CKD)-mediated arterial neointimal hyperplasia (NH), we utilized caspase(-/-) mice and induced NH in carotid artery in a CKD environment, and uremic sera-stimulated human vascular smooth muscle cells (VSMC). We made the following findings: (1) Caspase-1 inhibition corrected uremic sera-mediated downregulation of VSMC contractile markers, (2) CKD-promoted NH was attenuated in caspase(-/-) mice, (3) CKD-mediated downregulation of contractile markers was rescued in caspase null mice, and (4) expression of VSMC migration molecule alpha v beta 3 integrin was reduced in caspase(-/-) tissues. Our results suggested that caspase-1 pathway senses CKD metabolic danger signals. Further, CKD-mediated increase of contractile markers in VSMC and increased expression of VSMC migration molecule alpha v beta 3 integrin in NH formation were caspase-1 dependent. Therefore, caspase-1 is a novel therapeutic target for the suppression of CKD-promoted NH.

引用

页码：135 / 144

页数：10

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