MicroRNA-151 Attenuates Apoptosis of Endothelial Cells Induced by Oxidized Low-density Lipoprotein by Targeting Interleukin-17A (IL-17A)

Chen, Fan‐Feng; Ye, Xiaoning; Jiang, Haote; Zhu, Guanxia; Miao, Shouliang

doi:10.1007/s12265-020-10065-w

Cited by 21 publications

(13 citation statements)

References 34 publications

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“…In most cases, polygenic diseases, including atherosclerosis, develop when the expression of different combinations of candidate genes changes. As a result of a review of various publications, it seems that the approaches used to search for markers for the diagnosis and treatment of atherosclerosis, including miRNA, have not yet solved the problem of diagnosing and treating atherosclerosis (Chen et al, 2020;Ryu et al, 2020;Sun et al, 2020;You et al, 2020). In human, it is known about 7000 miRNA and more than 20,000 genes, and it is unknown how many miRNA and genes from them participate in the development of atherosclerosis (Byrne et al, 2014;Toba et al, 2014;Lu et al, 2018;Liu et al, 2020;Shi et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

In silico Prediction of miRNA Interactions With Candidate Atherosclerosis Gene mRNAs

et al. 2020

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The involvement of genes and miRNAs in the development of atherosclerosis is a challenging problem discussed in recent publications. It is necessary to establish which miRNAs affect the expression of candidate genes. We used known candidate atherosclerosis genes to predict associations. The quantitative characteristics of interactions of miRNAs with mRNA candidate genes were determined using the program, which identifies the localization of miRNA binding sites in mRNA, the free energy interaction of miRNA with mRNA. In mRNAs of GAS6 and NFE2L2 candidate genes, binding sites of 21 miRNAs and of 15 miRNAs, respectively, were identified. In IRS2 mRNA binding sites of 25 miRNAs were located in a cluster of 41 nt. In ADRB3, CD36, FASLG, FLT1, PLA2G7 , and PPARGC1A mRNAs, clusters of miR-466, ID00436.3p-miR, and ID01030.3p-miR BS were identified. The organization of overlapping miRNA binding sites in clusters led to their compaction and caused competition among the miRNAs. The binding of 53 miRNAs to the mRNAs of 14 candidate genes with free energy interactions greater than −130 kJ/mole was determined. The miR-619-5p was fully complementary to ADAM17 and CD36 mRNAs, ID01593.5p-miR to ANGPTL4 mRNA, ID01935.5p-miR to NFE2L2 , and miR-5096 to IL18 mRNA. Associations of miRNAs and candidate atherosclerosis genes are proposed for the early diagnosis of this disease.

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Section: Introductionmentioning

confidence: 99%

In silico Prediction of miRNA Interactions With Candidate Atherosclerosis Gene mRNAs

et al. 2020

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“…As miRNAs are emerging as promising therapeutic targets for drug development, 22 , 23 , 24 , 25 , 26 , 27 , 28 we reported downregulation of miR-30d in different cardiac hypertrophy models both in vivo and vitro , which implied that miR-30d may be a crucial molecular orchestrator and a promising therapeutic target for pathological cardiac hypertrophy. To investigate the therapeutic potential of miR-30d in the clinical situations, AAV9 expressing miR-30d was designed to treat established pathological cardiac hypertrophy.…”

Section: Discussionmentioning

confidence: 68%

Targeting miR-30d reverses pathological cardiac hypertrophy

et al. 2022

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“…miRNA can modulate gene expression at posttranscriptional level, and affect the phenotypes of ECs, thus impacting the progression of AS. [15][16][17] For example, miR-151 has been found to inhibit the apoptosis of ox-LDL-induced ECs by silencing IL-17A, thus alleviating the development of AS [16] ; miR-126-5p can enhance the viability of ECs by inhibiting Dlk1, thus alleviating the pathological changes of AS. [17] In the previous studies, miR-125a-3p has been reported to participate in modulating the pathogenesis of several human diseases, including cardiovascular diseases.…”

Section: Discussionmentioning

confidence: 99%

miR‐125a‐3p aggravates ox‐LDL‐induced HUVEC injury through BAMBI

Xia

Zeng

2022

J Biochem & Molecular Tox

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Atherosclerosis (AS) is a chronic inflammatory disease characterized by the formation of atherosclerotic plaque in the intima of arteries. Among the known regulators of atherosclerosis, microRNAs (miRNAs) have been reported to play critical roles in lipoprotein homeostasis and plaque formation. But the roles of microRNA‐125a‐3p (miR‐125a‐3p) in the pathogenesis of AS remain unknown. Human umbilical vein endothelial cells (HUVECs) were treated with oxidized low‐density lipoprotein (ox‐LDL) to construct the vascular injury model of AS pathogenesis in vitro. miR‐125a‐3p and BMP and activin membrane‐bound inhibitor (BAMBI) expression levels in HUVECs were then measured by quantitative real‐time polymerase chain reaction and western blot. The viability and apoptosis of HUVECs were analyzed by Cell Counting Kit‐8 assay, TUNEL assay, and flow cytometry, respectively. The relationship between BAMBI 3′‐untranslated region and miR‐125a‐3p was validated by dual luciferase reporter gene assay. miR‐125a‐3p expression was raised in HUVECs induced with ox‐LDL. In HUVECs, miR‐125a‐3p enhanced the effects of ox‐LDL treatment on repressing the viability and promoting the apoptosis of cells. Additionally, BAMBI was confirmed as a direct target of miR‐125a‐3p and BAMBI overexpression reversed the effects of miR‐125a‐3p on HUVECs. miR‐125a‐3p aggravates the dysfunction of HUVECs induced by ox‐LDL via BAMBI, which implies that miR‐125a‐3p is involved in the pathogenesis of AS.

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MicroRNA-151 Attenuates Apoptosis of Endothelial Cells Induced by Oxidized Low-density Lipoprotein by Targeting Interleukin-17A (IL-17A)

Cited by 21 publications

References 34 publications

In silico Prediction of miRNA Interactions With Candidate Atherosclerosis Gene mRNAs

In silico Prediction of miRNA Interactions With Candidate Atherosclerosis Gene mRNAs

Targeting miR-30d reverses pathological cardiac hypertrophy

miR‐125a‐3p aggravates ox‐LDL‐induced HUVEC injury through BAMBI

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