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半胱天冬酶-1在加速慢性肾病促进的颈动脉内膜增生中起关键作用。

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

作者信息

Ferrer Lucas M, Monroy Alexandra M, Lopez-Pastrana Jahaira, Nanayakkara Gayani, Cueto Ramon, Li Ya-Feng, Li Xinyuan, Wang Hong, Yang Xiao-Feng, Choi Eric T

机构信息

Centers for Metabolic Disease Research, Cardiovascular Research and Thrombosis Research, Lewis Katz School of Medicine, Temple University, 3500, North Broad Street, Philadelphia, PA, 19140, USA.

Department of Surgery, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.

出版信息

J Cardiovasc Transl Res. 2016 Apr;9(2):135-44. doi: 10.1007/s12265-016-9683-3. Epub 2016 Feb 29.

DOI:10.1007/s12265-016-9683-3
PMID:26928596
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5131710/
Abstract

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 αvβ3 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 αvβ3 integrin in NH formation were caspase-1 dependent. Therefore, caspase-1 is a novel therapeutic target for the suppression of CKD-promoted NH.

摘要

为了确定半胱天冬酶 -1在慢性肾脏病（CKD）介导的动脉内膜增生（NH）中是否起关键作用，我们使用了半胱天冬酶基因敲除（-/-）小鼠，并在CKD环境中诱导颈动脉内膜增生，同时研究了尿毒症血清刺激的人血管平滑肌细胞（VSMC）。我们有以下发现：（1）半胱天冬酶 -1抑制纠正了尿毒症血清介导的VSMC收缩标志物下调；（2）CKD促进的内膜增生在半胱天冬酶基因敲除（-/-）小鼠中减弱；（3）CKD介导的收缩标志物下调在半胱天冬酶基因敲除小鼠中得到挽救；（4）在半胱天冬酶基因敲除（-/-）组织中，VSMC迁移分子αvβ3整合素的表达降低。我们的结果表明，半胱天冬酶 -1途径感知CKD代谢危险信号。此外，CKD介导的VSMC中收缩标志物增加以及在NH形成中VSMC迁移分子αvβ3整合素表达增加是依赖半胱天冬酶 -1的。因此，半胱天冬酶 -1是抑制CKD促进的内膜增生的新治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43dc/5131710/b3e3fd746e49/nihms-830483-f0006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43dc/5131710/c9ee6e34c312/nihms-830483-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43dc/5131710/c796487cb674/nihms-830483-f0003.jpg
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