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微小RNA-301a-3p通过靶向KLF7增加氧化型低密度脂蛋白诱导的人脐静脉内皮细胞中的氧化应激、炎症和细胞凋亡。

MicroRNA-301a-3p increases oxidative stress, inflammation and apoptosis in ox-LDL-induced HUVECs by targeting KLF7.

作者信息

Jiang Huiqiong, Lv Jiaren

机构信息

Cardiac Function Examination Room, Quanzhou First Hospital, Quanzhou, Fujian 362000, P.R. China.

出版信息

Exp Ther Med. 2021 Jun;21(6):569. doi: 10.3892/etm.2021.10001. Epub 2021 Mar 29.

DOI:10.3892/etm.2021.10001
PMID:33850541
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8027757/
Abstract

Arteriosclerotic cardiovascular disease is an inflammatory disease of ischemia or endothelial dysfunction caused by atherosclerosis, thereby causing high mortality. The viability and apoptosis of human umbilical vein endothelial cells (HUVECs) following oxidized low-density lipoprotein (ox-LDL) induction or transfection was detected by Cell Counting Kit-8 (CCK-8) assay and flow cytometry analysis. MicroRNA (miR)-301a-3p and Krueppel-like factor 7 (KLF7) mRNA expression was determined by reverse transcription-quantitative PCR (RT-qPCR). The levels of monocyte chemoattractant protein-1 (MCP-1) and IL-6, activities of reactive oxygen species and superoxide dismutase and lactate dehydrogenase leakage were analyzed by respective commercial assay kits. The protein expression of IL-6, MCP-1, Bcl2, Bax, poly (ADP-ribose) polymerase (PARP), cleaved PARP, pro-caspase3 and cleaved caspase-3 was detected by western blotting. miR-301a-3p expression is highly expressed in ox-LDL-induced HUVECs. miR-301a-3p is also a target of KLF7. Inhibition of miR-301a-3p suppressed oxidative stress, inflammation and apoptosis in ox-LDL-induced HUVECs, which was reversed by KLF7 inhibition. In conclusion, miR-301a-3p promotes oxidative stress, inflammation and apoptosis in ox-LDL-induced HUVECs via decreasing KLF7 expression.

摘要

动脉粥样硬化性心血管疾病是一种由动脉粥样硬化引起的缺血或内皮功能障碍的炎症性疾病，从而导致高死亡率。通过细胞计数试剂盒-8（CCK-8）检测和流式细胞术分析，检测氧化型低密度脂蛋白（ox-LDL）诱导或转染后人脐静脉内皮细胞（HUVECs）的活力和凋亡情况。通过逆转录定量PCR（RT-qPCR）测定微小RNA（miR）-301a-3p和Krüppel样因子7（KLF7）mRNA的表达。分别使用商业检测试剂盒分析单核细胞趋化蛋白-1（MCP-1）和IL-6的水平、活性氧和超氧化物歧化酶的活性以及乳酸脱氢酶泄漏情况。通过蛋白质印迹法检测IL-6、MCP-1、Bcl2、Bax、聚（ADP-核糖）聚合酶（PARP）、裂解的PARP、前半胱天冬酶3和裂解的半胱天冬酶3的蛋白表达。miR-301a-3p在ox-LDL诱导的HUVECs中高表达。miR-301a-3p也是KLF7的一个靶点。抑制miR-301a-3p可抑制ox-LDL诱导的HUVECs中的氧化应激、炎症和凋亡，而KLF7抑制可逆转这种作用。总之，miR-301a-3p通过降低KLF7表达促进ox-LDL诱导的HUVECs中的氧化应激、炎症和凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8672/8027757/737273f41134/etm-21-06-10001-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8672/8027757/b2c47c348c6a/etm-21-06-10001-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8672/8027757/b2e563da8938/etm-21-06-10001-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8672/8027757/797901d19412/etm-21-06-10001-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8672/8027757/21aa28684cac/etm-21-06-10001-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8672/8027757/b4d0b899a9a3/etm-21-06-10001-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8672/8027757/737273f41134/etm-21-06-10001-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8672/8027757/b2c47c348c6a/etm-21-06-10001-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8672/8027757/b2e563da8938/etm-21-06-10001-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8672/8027757/797901d19412/etm-21-06-10001-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8672/8027757/21aa28684cac/etm-21-06-10001-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8672/8027757/b4d0b899a9a3/etm-21-06-10001-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8672/8027757/737273f41134/etm-21-06-10001-g05.jpg

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