Cao Chen, Zhen Wei, Yu Haibin, Zhang Li, Liu Yiling
Interventional Department, The Second Affiliated Hospital, Zhengzhou University, Zhengzhou 450014, China.
President's Office, The Second Affiliated Hospital, Zhengzhou University, Zhengzhou 450014, China.
Open Life Sci. 2021 Dec 20;16(1):1303-1312. doi: 10.1515/biol-2021-0126. eCollection 2021.
The purpose of this study is to observe the potential value and underlying mechanism of the metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)/miR-143 axis in ISR. A total of 150 participants were enrolled, including 100 patients (observation group) with coronary heart disease who underwent stent implantation in the Department of Cardiology of our hospital between January 2018 and January 2020, and 50 healthy people (control group) concurrently underwent a physical examination. Serum MALAT1 and miR-143 levels were detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Tumor necrosis factor-α (TNF-α; 10 ng/mL) induced human vascular smooth muscle cells (HVSMCs). MALAT1 increased while miR-143 decreased in the observation group versus the control group ( < 0.001). The non-restenosis group had significantly elevated MALAT1 expression while decreased miR-143 expression than the restenosis group ( < 0.001). The areas under the curves of the expression of MALAT1 and miR-143 in predicting restenosis were 0.917 and 0.881, respectively. Following si-MALAT1 transfection, HVSMC multiplication and invasiveness decreased significantly ( < 0.05). miR-143-inhibitor was observed to upregulate the luciferase activity of MALAT1-WT ( < 0.05). MALAT1 is highly expressed in patients with ISR while miR-143 is decreased, and the MALAT1/miR-143 axis is a potential pathway to modulate the multiplication and invasiveness of HVSMCs.
本研究旨在观察转移相关肺腺癌转录本1（MALAT1）/miR-143轴在支架内再狭窄（ISR）中的潜在价值及潜在机制。共纳入150名参与者，包括100例冠心病患者（观察组），于2018年1月至2020年1月在我院心内科接受支架植入术，以及50名同时进行体检的健康人（对照组）。采用定量逆转录聚合酶链反应（qRT-PCR）检测血清MALAT1和miR-143水平。用肿瘤坏死因子-α（TNF-α；10 ng/mL）诱导人血管平滑肌细胞（HVSMCs）。与对照组相比，观察组MALAT1升高而miR-143降低（<0.001）。与再狭窄组相比，非再狭窄组MALAT1表达显著升高而miR-143表达降低（<0.001）。MALAT1和miR-143表达预测再狭窄的曲线下面积分别为0.917和0.881。转染si-MALAT1后，HVSMC增殖和侵袭能力显著降低（<0.05）。观察到miR-143抑制剂上调MALAT1-WT的荧光素酶活性（<0.05）。MALAT1在ISR患者中高表达而miR-143降低，且MALAT1/miR-143轴是调节HVSMCs增殖和侵袭的潜在途径。
