Evidence map›Paper›PMID 33970415›Full record

ArticleMolecular biotechnology2021

Effect of miR-126 on the Proliferation and Migration of Vascular Smooth Muscle Cells in Aortic Aneurysm Mice Under PI3K/AKT/mTOR Signaling Pathway.

Changpin Huang, Xin Fang, Xupin Xie, Yongchang Liu, Dong Xu, Xiaohu Meng, Jianyun Long

Abstract read
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In one paragraph

Article in Molecular biotechnology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 50% of its field
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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Irisin protects against atherosclerosis in ApoEMolecular and cellular biochemistry · 2026
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4 · The record

Corrections and comments

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 at 1 institution in 1 country.

Changpin Huang *Department of Vascular Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, 310006, Zhejiang Province, China.
Xin Fang *Department of Vascular Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, 310006, Zhejiang Province, China. fangxin111@163.com.ORCID http://orcid.org/0000-0001-7378-5791
Xupin XieDepartment of Vascular Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, 310006, Zhejiang Province, China.
Yongchang LiuDepartment of Vascular Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, 310006, Zhejiang Province, China.
Dong XuDepartment of Vascular Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, 310006, Zhejiang Province, China.
Xiaohu MengDepartment of Vascular Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, 310006, Zhejiang Province, China.
Jianyun LongDepartment of Vascular Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, 310006, Zhejiang Province, China.
Hangzhou First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This paper is to investigate the expression changes of Phosphatidylinositol-3 Kinase (PI3K), protein kinase B (AKT), and Mammalian Target of Rapamycin (mTOR) in Vascular Smooth Muscle Cells (VSMCs) of aortic aneurysm mice, and to analyze the mechanism of VSMCs proliferation and migration. Aortic VSMCs cells were cultured using BALB/c mice as the research object. VSMCs were identified using artificial intelligence-based digital microscopy equipment, and liposome-transfected VSMCs experiments were performed. Real-time PCR was used for the mRNA expression levels of miR-126 and Phosphatase and Tensin Homolog (PTEN). Western blot was used for the protein expression levels of PTEN, PI3K, AKT, and mTOR. The cultured cells were identified as mouse VSMCs using digital microscopes based on artificial intelligence. Compared with the normal group, the expression of miR-126 and PTEN mRNA in the model group were significantly increased and reduced, respectively. Compared with the model group, the expression level of miR-126 and PTEN mRNA in the inhibitor group were significantly reduced and increased, respectively. Compared with the model group, the expression of miR-126 and PTEN mRNA in the ursolic acid group was significantly reduced and increased, respectively. After liposome transfection, compared with the normal group, the expression of PTEN protein in the model group was significantly reduced, and the expression of PI3K protein was significantly increased. Compared with the model group, the expression of PTEN protein was significantly increased and the expression of PI3K protein was significantly decreased in the transfection group. Compared with the control group, the expression of PI3K, AKT and mTOR protein in the model group was significantly increased. Compared with the model group, the expression of PI3K, AKT, and mTOR protein in the ursolic acid group was significantly reduced. The expressions of PI3K, AKT and mTOR protein in PI3K inhibitor group and AKT inhibitor group were significantly reduced. In conclusion, ursolic acid can inhibit the proliferation and migration of VSMCs in aortic aneurysm mice through the miR-126/PTEN/PI3K/AKT/mTOR signaling pathway. Furthermore, PTEN gene and miR-126 negatively regulate PI3K/AKT/mTOR and PTEN/PI3K/AKT/mTOR signaling pathway, respectively .

Indexed as

AnimalsAortic AneurysmArtificial IntelligenceCell MovementCell ProliferationCells, CulturedDisease Models, AnimalHumansLiposomesMaleMiceMice, Inbred BALB CMicroRNAsMuscle, Smooth, VascularMyocytes, Smooth MusclePhosphatidylinositol 3-KinaseLiposomesMicroRNAsMIRN126 microRNA, humanPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanTriterpenesUrsolic AcidArtificial intelligenceInfectious aortic aneurysmmiR-126PI3K/AKT/mTORVSMCs

Identifiers

PMID33970415
OpenAlexW3160839396

What OpenQuestion holds

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Registered trials

None linked

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 OpenQuestion graph.