[药物洗脱支架植入术后冠心病患者基因表达与支架内再狭窄风险的关联及其对人血管内皮细胞的影响和机制]
[Association of gene expression with the risk of in-stent restenosis in patients with coronary artery disease after drug-eluting stent implantation and the effects and mechanisms of on human vascular endothelial cells].
作者信息
Liu T F, Lin T, Ren L H, Li G P, Peng J J
出版信息
Beijing Da Xue Xue Bao Yi Xue Ban. 2020 Oct 18;52(5):856-862. doi: 10.19723/j.issn.1671-167X.2020.05.010.
OBJECTIVE
To elucidate the correlation between CKLF-like marvel transmembrane domain containing member () gene and the risk of in-stent restenosis (ISR) with coronary artery disease (CAD) patients and to detect the effects and mechanisms of -stimulated genes on human vascular endothelial cells (ECs) proliferation and migration.
METHODS
A total of 124 hospitalized patients in Shijitan Hospital were enrolled in this study. All the CAD patients were detected with platelet reactivity and grouped into two groups according to platelet reactivity; ISR was conformed by coronary angiography; RT-PCR method was used to detect gene expression; The over expression, reduction and control EC lines were established; Cell count, MTT, Brdu and flow cytometry methods were used to detect the proliferation of ECs, scratch and transwell experiments to test the migration of ECs, Western blot was used to detect signal path expressions.
RESULTS
gene expression in HAPR (High on aspirin platelet reactivity) group was 1.72 times compared with No-HAPR group, which was significantly higher than No-HAPR group. HAPR group ISR rate was 25.8% (8 cases), the incidence of No-HAPR ISR group was 9.7% (9 cases), and the results showed that in HAPR group, the incidence of ISR was significantly higher than that in No-HAPR group (=0.04, =0.04, 95%=1.16－7.52), which showed that gene was significantly correlated with the risk of ISR. In HAPR group ISR rate was 25.8% (8 cases), the incidence of ISR in No-HAPR group was 9.7% (9 cases), and the results showed that the risk of ISR in HAPR group was significantly higher than that in No-HAPR group. All the results showed that was significantly correlated with the risk of ISR in CAD patients ( < 0.05). overexpression inhibited the proliferation and migration ability of ECs ( < 0.05), PI3K/Akt signaling pathways were involved in the role of regulation on ECs.
CONCLUSION
Our results revealed that gene was closely related with ISR, overexpression may repress ECs proliferation and migration through regulating PI3K-Akt signaling.
目的
阐明含卷曲螺旋样膜联蛋白跨膜结构域成员（）基因与冠心病（CAD）患者支架内再狭窄（ISR）风险之间的相关性，并检测刺激基因对人血管内皮细胞（ECs）增殖和迁移的影响及机制。
方法
选取世纪坛医院124例住院患者纳入本研究。对所有CAD患者检测血小板反应性，并根据血小板反应性分为两组；通过冠状动脉造影确诊ISR；采用RT-PCR法检测基因表达；建立基因过表达、降低表达及对照的EC细胞系；采用细胞计数、MTT、Brdu及流式细胞术检测ECs增殖，划痕及transwell实验检测ECs迁移，Western blot检测信号通路表达。
结果
高阿司匹林反应性血小板组（HAPR）基因表达较非HAPR组高1.72倍，差异有统计学意义。HAPR组ISR发生率为25.8%（8例），非HAPR组ISR发生率为9.7%（9例），结果显示HAPR组ISR发生率显著高于非HAPR组（=0.04，=0.04，95%可信区间=1.16－7.52），表明基因与ISR风险显著相关。HAPR组ISR发生率为25.8%（8例），非HAPR组ISR发生率为9.7%（9例），结果显示HAPR组ISR风险显著高于非HAPR组。所有结果表明，与CAD患者ISR风险显著相关（<0.05）。基因过表达抑制ECs增殖和迁移能力（<0.05），PI3K/Akt信号通路参与对ECs的调控作用。
结论
研究结果表明，基因与ISR密切相关，基因过表达可能通过调节PI3K-Akt信号通路抑制ECs增殖和迁移。
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