Evidence map›Paper›PMID 38910413›Full record

ArticleCurrent vascular pharmacology2024

MiR-199a-5p Deficiency Promotes Artery Restenosis in Peripheral Artery Disease by Regulating ASMCs Function

Duan Liu, Yexiang Jing, Guiyan Peng, Litai Wei, Liang Zheng, Guangqi Chang, Mian Wang

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Article in Current vascular pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Duan LiuDivision of Vascular Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Yexiang JingDivision of Vascular Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Guiyan PengDivision of Vascular Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Litai WeiDivision of Vascular Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Liang ZhengDivision of Vascular Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Guangqi ChangDivision of Vascular Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Mian WangDivision of Vascular Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.

Funding

National Natural Science Foundation of China 81970416,81670441,81970416,81670441National Natural Science Foundation of China (NSFC) 81670441 and 81970416
6 · The paper itself

Abstract

backgroundRestenosis (RS) poses a significant concern, leading to recurrent ischemia and the potential for amputation following intraluminal angioplasty in the treatment of Peripheral Artery Disease (PAD). Through microRNA microarray analysis, the study detected a significant downregulation of miR-199a-5p within arterial smooth muscle cells (ASMCs) associated with RS.

objectiveThis research aims to explore the possible function and the underlying mechanisms of miR-199a-5p in the context of RS.

methodsPrimary ASMCs were extracted from the femoral arteries of both healthy individuals and patients with PAD or RS. The expression levels of miR-199a-5p were assessed using both qRT-PCR and in situ hybridization techniques. To examine the impacts of miR-199a-5p, a series of experiments were performed, including flow cytometry, TUNEL assay, EdU assay, CCK8 assay, Transwell assay, and wound closure assay. A rat carotid balloon injury model was employed to elucidate the mechanism through which miR-199a-5p mitigated neointimal hyperplasia.

resultsMiR-199a-5p exhibited downregulation in RS patients and was predominantly expressed within ASMCs. Elevated the expression of miR-199a-5p resulted in an inhibitory effect of proliferation and migration in ASMCs. Immunohistochemistry and a dual-luciferase reporter assay uncovered that RS exhibited elevated expression levels of both HIF-1α and E2F3, and they were identified as target genes regulated by miR-199a-5p. The co-transfection of lentiviruses carrying HIF-1α and E2F3 alongside miR-199a-5p further elucidated their role in the cellular responses mediated by miR-199a-5p.

conclusionMiR-199a-5p exhibits promise as a prospective therapeutic target for RS since it alleviates the condition by inhibiting the proliferation and migration of ASMCs

Indexed as

Cell MovementCell ProliferationDisease Models, AnimalE2F3 Transcription FactorHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMuscle, Smooth, VascularMyocytes, Smooth MusclePeripheral Arterial DiseaseRats, Sprague-DawleyAgedAngioplasty, BalloonAnimalsApoptosisCarotid Artery InjuriesCase-Control StudiesE2F3 protein, humanE2F3 Transcription FactorHIF1A protein, humanHif1a protein, ratHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsmirn199 microRNA, humanMIRN199 microRNA, ratArterial Smooth Muscle CellsE2F3.HIF-1αmiR-199a-5pPeripheral Artery DiseaseRestenosis

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.