RETRACTED: PRDM16 Upregulation Induced by MicroRNA-448 Inhibition Alleviates Atherosclerosis via the TGF-β Signaling Pathway Inactivation

Liu, Dongxing; Song, Jiantao; Ji, Xianfei; Liu, Zunqi; Li, Tao; Hu, Bo

doi:10.3389/fphys.2020.00846

Cited by 9 publications

(5 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, PRDM16 is enriched in GTEx arterial tissues and was identified as a key driver gene in STARNET artery tissue, consistent with our scATAC data. PRDM16 regulates TGF-beta signaling 84 through direct interactions with Smad 85 and SKI 86 proteins, both of which are associated with CAD 13 . PRDM16 may play key roles in endothelial cells in arterial flow recovery 87 .…”

Section: Discussionmentioning

confidence: 99%

Cell-specific chromatin landscape of human coronary artery resolves regulatory mechanisms of disease risk

Turner

Mosquera

et al. 2021

Preprint

View full text Add to dashboard Cite

Coronary artery disease (CAD) is a complex inflammatory disease involving genetic influences across several cell types. Genome-wide association studies (GWAS) have identified over 170 loci associated with CAD, where the majority of risk variants reside in noncoding DNA sequences impacting cis-regulatory elements (CREs). Here, we applied single-cell ATAC-seq to profile 28,316 cells across coronary artery segments from 41 patients with varying stages of CAD, which revealed 14 distinct cellular clusters. We mapped ~320,000 accessible sites across all cells, identified cell type-specific elements, transcription factors, and prioritized functional CAD risk variants via quantitative trait locus and sequence-based predictive modeling. We identified a number of candidate mechanisms for smooth muscle cell transition states and identified putative binding sites for risk variants. We further employed DNA element to gene linkage to nominate disease-associated key driver transcription factors such as PRDM16 and TBX2. This single cell atlas provides a critical step towards interpreting cis-regulatory mechanisms in the vessel wall across the continuum of CAD risk.

show abstract

Section: Discussionmentioning

confidence: 99%

Cell-specific chromatin landscape of human coronary artery resolves regulatory mechanisms of disease risk

Turner

Mosquera

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…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). As a rule, in publications several miRNA and some candidate genes are studied, so the combination of such attempts is large (Wang C. et al, 2020;Wang M. et al, 2020;Zhang et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

In silico Prediction of miRNA Interactions With Candidate Atherosclerosis Gene mRNAs

et al. 2020

View full text Add to dashboard Cite

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.

show abstract

“…Wang et al indicated that miR-377-3p inhibited atherosclerosis-associated vascular smooth muscle cell proliferation and migration through targeting neuropilin2 [ 19 ]. Liu et al demonstrated that PRDM16 upregulation induced by miR-448 inhibition alleviates atherosclerosis via the TGF-beta signaling pathway inactivation [ 20 ]. It was indicated that miR-552 was tightly involved in the development of different kinds of cancers.…”

Section: Discussionmentioning

confidence: 99%

ATF4 promotes brain vascular smooth muscle cells proliferation, invasion and migration by targeting miR-552-SKI axis

Feng

Zhou

et al. 2022

PLoS ONE

View full text Add to dashboard Cite

Background Studies have indicated vascular smooth muscle cells (VSMCs) played a crucial role in atherosclerosis and microRNAs (miRNAs) played key roles in biological functions of VSMCs. Whereas, the potential function and mechanism of miR-552 in VSMCs remains unclear. Our aim was to explore the role of miR-552 on VSMCs and underlying mechanism. Material/Methods MTT assay and transwell assay were used to measure the proliferation, invasion, and migration of human brain VSMCs (HBVSMCs) and mice VSMCs (mVSMCs), respectively. Bioinformatics tools and luciferase assay were adopted to verify the association between miR-552 and SKI. Rescue experiments were employed to assess the interaction of miR-552 and SKI in modulating biological functions in HBVSMCs and mVSMCs. The expression level of transcription factors (TFs)was measured via qRT-PCR assay. The effect of ATF4 on miR-552 and SKI expression was tested by qRT-PCR or western blot assay. Finally, chromatin immunoprecipitation (ChIP) assay and JASPAR databases were used to analyze the regulatory linkage between ATF4 and miR-552. Results We found that miR-552 was upregulated in HBVSMCs treated with PDGF-bb and miR-552 overexpression could promote proliferation, invasion, and migration of HBVSMCs and mVSMCs, whereas, miR-552 knockdown had the opposite impact. In addition, we also found that SKI was a direct target of miR-552, which reversed miR-552-mediated proliferation, invasion, and migration in HBVSMCs and mVSMCs. Furthermore, we also discovered that miR-552 overexpression promoted the effects of ATF4 elevation on proliferation, migration and invasion of HBVSMCs and mVSMCs, but, miR-552 decline had the opposite impact. Conclusions ATF4-miR-552-SKI axis played critical roles in the proliferation and migration of HBVSMCs and mVSMCs, which were closely involved in atherosclerosis (AS). Therefore, our findings might offer a novel therapeutic target for AS.

show abstract

RETRACTED: PRDM16 Upregulation Induced by MicroRNA-448 Inhibition Alleviates Atherosclerosis via the TGF-β Signaling Pathway Inactivation

Cited by 9 publications

References 43 publications

Cell-specific chromatin landscape of human coronary artery resolves regulatory mechanisms of disease risk

Cell-specific chromatin landscape of human coronary artery resolves regulatory mechanisms of disease risk

In silico Prediction of miRNA Interactions With Candidate Atherosclerosis Gene mRNAs

ATF4 promotes brain vascular smooth muscle cells proliferation, invasion and migration by targeting miR-552-SKI axis

Contact Info

Product

Resources

About