Evidence map›Paper›PMID 31918758›Full record

ArticleStem cell research & therapy2020

IGF-1 enhances BMSC viability, migration, and anti-apoptosis in myocardial infarction via secreted frizzled-related protein 2 pathway.

Mingzhuo Lin, Xinyue Liu, Haoxiao Zheng, Xiaohui Huang, Yu Wu, Anqing Huang, Hailan Zhu, Yunzhao Hu, Weiyi Mai, Yuli Huang

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 3 pooled it
6.8field-weighted citation impact, top 2% 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

60 citing papers in PubMed, 3 syntheses or guidelines pooled it, 115 citations in OpenAlex.

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  4. Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 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

10 authors at 2 institutions in 2 countries.

Mingzhuo LinDepartment of Cardiology, Shunde Hospital, Southern Medical University (the first people's hospital of Shunde), Jiazhi Road, Lunjiao Town, Shunde District, Foshan, 528300, People's Republic of China.
Xinyue LiuDepartment of Cardiology, Shunde Hospital, Southern Medical University (the first people's hospital of Shunde), Jiazhi Road, Lunjiao Town, Shunde District, Foshan, 528300, People's Republic of China.
Haoxiao ZhengDepartment of Cardiology, Shunde Hospital, Southern Medical University (the first people's hospital of Shunde), Jiazhi Road, Lunjiao Town, Shunde District, Foshan, 528300, People's Republic of China.
Xiaohui HuangDepartment of Cardiology, Shunde Hospital, Southern Medical University (the first people's hospital of Shunde), Jiazhi Road, Lunjiao Town, Shunde District, Foshan, 528300, People's Republic of China.
Yu WuDepartment of Cardiology, Shunde Hospital, Southern Medical University (the first people's hospital of Shunde), Jiazhi Road, Lunjiao Town, Shunde District, Foshan, 528300, People's Republic of China.
Anqing HuangDepartment of Cardiology, Shunde Hospital, Southern Medical University (the first people's hospital of Shunde), Jiazhi Road, Lunjiao Town, Shunde District, Foshan, 528300, People's Republic of China.
Hailan ZhuDepartment of Cardiology, Shunde Hospital, Southern Medical University (the first people's hospital of Shunde), Jiazhi Road, Lunjiao Town, Shunde District, Foshan, 528300, People's Republic of China.
Yunzhao HuDepartment of Cardiology, Shunde Hospital, Southern Medical University (the first people's hospital of Shunde), Jiazhi Road, Lunjiao Town, Shunde District, Foshan, 528300, People's Republic of China.
Weiyi MaiDepartment of Cardiology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, People's Republic of China.
Yuli HuangDepartment of Cardiology, Shunde Hospital, Southern Medical University (the first people's hospital of Shunde), Jiazhi Road, Lunjiao Town, Shunde District, Foshan, 528300, People's Republic of China. hyuli821@smu.edu.cn.ORCID 0000-0001-5104-567X
The First People's Hospital of Shunde · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBone marrow mesenchymal stem cell (BMSC) transplantation represents a promising therapeutic strategy for ischemic heart disease. However, its effects are hampered by the poor viability of transplanted cells and the hostile microenvironment of the ischemic region. Insulin-like growth factor-1 (IGF-1) is an important paracrine growth factor of BMSC and plays an important role in the properties of BMSC. Here, we investigated whether overexpressing IGF-1 could enhance the BMSC viability, migration, anti-apoptosis, and protective effects of cardiomyocytes, and explore the underlying mechanisms' focus on the role of the AKT/secreted frizzled-related protein 2 (SFRP2)/β-catenin pathway.

methodsWe constructed BMSCs overexpressing insulin-like growth factor-1 (BMSCs-IGF-1) or empty vector (BMSCs-NC) using lentivirus, and evaluated cell survival, proliferation, and migration under normoxic and hypoxic conditions. Co-culture of rat cardiomyoblasts with BMSCs was performed to explore the paracrine effect of BMSCs-IGF-1 for rescuing cardiomyoblasts under hypoxia. Transplantation of BMSCs in acute myocardial infarction rats was used to explore the effect of BMSCs-IGF-1 therapy.

resultsBMSCs-IGF-1 exhibited a higher cell proliferation rate, migration capacity, and stemness, and were more resistant to apoptosis under hypoxia. Overexpression of IGF-1 upregulated the expression of total and nuclear β-catenin via the AKT-secreted frizzled-related protein 2 (SFRP2) pathway, which enhanced cell survival. Inhibition of AKT or SFRP2 knockdown by siRNA significantly antagonized the effect of IGF-1 and decreased the expression of β-catenin. The expression of β-catenin target genes, including cyclin D1 and c-Myc, were accordingly decreased. Moreover, BMSCs-IGF-1 could rescue cardiomyoblasts from hypoxia-induced apoptosis and preserve cell viability under hypoxia. Transplantation of BMSCs-IGF-1 into myocardial infarction rats greatly reduced infarct volume than BMSCs-NC, with significantly greater expression of SFRP2 and β-catenin.

conclusionsThese results suggest that in BMSCs overexpressing IGF-1, SFRP2 is an important mediator for the enhancement of stem cell viability via activating, rather than antagonizing, the Wnt/β-catenin pathway.

Indexed as

AnimalsApoptosisbeta CateninCell MovementCells, CulturedCell SurvivalInsulin-Like Growth Factor IMaleMembrane ProteinsMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMyocardial InfarctionMyocytes, CardiacProto-Oncogene Proteins c-aktRatsRats, Sprague-Dawleybeta CateninCtnnb1 protein, ratInsulin-Like Growth Factor IMembrane ProteinsProto-Oncogene Proteins c-aktSecreted Frizzled-Related ProteinsSfrp2 protein, ratBone marrow mesenchymal stem cellInsulin-like growth factor-1Myocardial infarctionSecreted frizzled-related protein 2

Identifiers

PMID31918758
PMCPMC6953226
OpenAlexW3004882858

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LicenceCC BY
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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.