Evidence map›Paper›PMID 38984951›Full record

ArticleJournal of cellular and molecular medicine2024

Upregulation of circ-IGF1R increased therapeutic effect of hypoxia-pretreated ADSC-derived extracellular vesicle by regulating miR-503-5p/HK2/VEGFA axis.

Rongfeng Shi, Pengfei Jia, Suming Zhao, Hongxin Yuan, Jiahai Shi, Hui Zhao

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Review
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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

6 authors.

Rongfeng ShiDepartment of Interventional and Vascular Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, P.R. China.
Pengfei JiaDepartment of Interventional and Vascular Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, P.R. China.
Suming ZhaoDepartment of Interventional and Vascular Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, P.R. China.
Hongxin YuanDepartment of Interventional and Vascular Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, P.R. China.
Jiahai ShiDepartment of Thoracic Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, P.R. China.
Hui ZhaoDepartment of Interventional and Vascular Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, P.R. China.ORCID 0000-0002-9221-6831

Funding

Innovation Team Project of Affiliated Hospital of Nantong University XNBHCX31773Jiangsu Provincial Research Hospital YJXYY202204Natural Science Foundation of Jiangsu Province of  China BK20180946the National Natural Science Foundation of China 82102167the National Natural Science Foundation of China 82272093the National Natural Science Foundation of China 82370253the Science Foundation of China Postdoctoral 2019M651928
6 · The paper itself

Abstract

Diabetes mellitus is a major cause of blindness and chronic ulcers in the working-age population worldwide. Wound healing is deeply dependent on neovascularization to restore blood flow. Former research has found that differentially expressed circular RNAs (circRNAs) are associated with hyperglycaemia-induced endothelial cell damage, and hypoxia-pretreated adipose-derived stem cells (ADSCs)-extracellular vesicle (HEV) transplants have a more therapeutic effect to enhance wound healing in diabetic mice by delivery circRNA. The current investigation employed high-throughput sequencing to identify circRNAs that are abnormally expressed between EV and HEV. The regulatory mechanism and predicted targets of one differentially expressed circRNA, circ-IGF1R, were investigated utilizing bioinformatics analyses, luciferase reporter assays, angiogenic differentiation assays, flow cytometric apoptosis analysis and RT-qPCR. Circ-IGF1R expression increased in HEV, and downregulation of circ-IGF1R suppressed and reversed the promotion effect of HEV on angiogenesis in ulcerated tissue. Bioinformatics analyses and luciferase reporter assays confirmed that miR-503-5p was the downstream target of circ-IGF1R, and inhibiting miR-503-5p restored the promotion effect of HEV on angiogenesis after circ-IGF1R silence. The study also found that miR-503-5p can interact with 3'-UTR of both HK2 and VEGFA. Overexpression of HK2 or VEGFA restored the promotion effect of HExo on angiogenesis after circ-IGF1R silence. Overexpression miR-503-5p or silence HK2/VEGFA reversed the protective effect of circ-IGF1R to MLMECs angiogenic differentiation. Overexpression of circ-IGF1R increased the protective effect of HEV on the promotion of wound healing in mice with diabetes. Circ-IGF1R promotes HIF-1α expression through miR-503-5p sponging. Our data demonstrate that circ-IGF1R overexpression EVs from ADSCs suppress high glucose-induced endothelial cell damage by regulating miR-503-5p/HK2/VEGFA axis.

Indexed as

Extracellular VesiclesMicroRNAsReceptor, IGF Type 1RNA, CircularVascular Endothelial Growth Factor AAnimalsCell HypoxiaGene Expression RegulationHumansMaleMiceNeovascularization, PhysiologicSignal TransductionStem CellsUp-RegulationWound HealingIGF1R protein, humanMicroRNAsReceptor, IGF Type 1RNA, CircularVascular Endothelial Growth Factor Acirc‐IGF1Rextracellular vesicleHK2miR‐503‐5pVEGFA

Identifiers

PMID38984951
PMCPMC11234642

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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 OpenQuestion graph.