Evidence map›Paper›PMID 33547700›Full record

ArticleStem cells (Dayton, Ohio)2021

SMAD-specific E3 ubiquitin ligase 2 promotes angiogenesis by facilitating PTX3 degradation in MSCs from patients with ankylosing spondylitis.

Mengjun Ma, Wen Yang, Zhaopeng Cai, Peng Wang, Hongyu Li, Rujia Mi, Yuhang Jiang, Zhongyu Xie, Pengfei Sui, Yanfeng Wu and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Mengjun MaDepartment of Orthopedics, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong, People's Republic of China.
Wen YangDepartment of Orthopedics, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong, People's Republic of China.
Zhaopeng CaiDepartment of Orthopedics, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong, People's Republic of China.
Peng WangDepartment of Orthopedics, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong, People's Republic of China.
Hongyu LiDepartment of Orthopedics, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong, People's Republic of China.
Rujia MiCenter for Biotherapy, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong, People's Republic of China.
Yuhang JiangDepartment of Orthopedics, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong, People's Republic of China.
Zhongyu XieDepartment of Orthopedics, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong, People's Republic of China.
Pengfei SuiState Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, People's Republic of China.
Yanfeng WuCenter for Biotherapy, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong, People's Republic of China.
Huiyong ShenDepartment of Orthopedics, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong, People's Republic of China.ORCID 0000-0003-0638-0182
Sun Yat-sen University · CNCenter for Excellence in Molecular Cell Science · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulated angiogenesis of mesenchymal stem cells (MSCs) is closely related to inflammation and disrupted bone metabolism in patients with various autoimmune diseases. However, the role of MSCs in the development of abnormal angiogenesis in patients with ankylosing spondylitis (AS) remains unclear. In this study, we cultured human umbilical vein endothelial cells (HUVECs) with bone marrow-derived MSCs from patients with AS (ASMSCs) or healthy donors (HDMSCs) in vitro. Then, the cocultured HUVECs were assayed using a cell counting kit-8 (CCK-8) to evaluate the cell proliferation. A wound healing assay was performed to investigate cell migration, and a tube formation assay was conducted to determine the angiogenesis efficiency. ASMSCs exhibited increased angiogenesis, and increased expression of SMAD-specific E3 ubiquitin ligase 2 (Smurf2) in MSCs was the main cause of abnormal angiogenesis in patients with AS. Downregulation of Smurf2 in ASMSCs blocked angiogenesis, whereas overexpression of Smurf2 in HDMSCs promoted angiogenesis. The pro-angiogenic effect of Smurf2 was confirmed by the results of a Matrigel plug assay in vivo. By functioning as an E3 ubiquitin ligase in MSCs, Smurf2 regulated the levels of pentraxin 3 (PTX3), which has been shown to suppress angiogenesis through the PTX3-fibroblast growth factor 2 pathway. Moreover, Smurf2 transcription was regulated by activating transcription factor 4-induced endoplasmic reticulum stress. In conclusion, these results identify novel roles of Smurf2 in negatively regulating PTX3 stability and promoting angiogenesis in ASMSCs.

Indexed as

Activating Transcription Factor 4Cell MovementCoculture TechniquesC-Reactive ProteinEndoplasmic Reticulum StressFibroblast Growth Factor 2Gene Expression Regulation, DevelopmentalHealthy VolunteersHumansHuman Umbilical Vein Endothelial CellsMesenchymal Stem CellsNeovascularization, PathologicPentraxinsSerum Amyloid P-ComponentSpondylitis, AnkylosingUbiquitin-Protein LigasesActivating Transcription Factor 4C-Reactive ProteinFibroblast Growth Factor 2PentraxinsSerum Amyloid P-ComponentSMURF2 protein, humanUbiquitin-Protein Ligasesangiogenesisarthritisautoimmune diseasemesenchymal stem cells (MSCs)tube formation

Identifiers

PMID33547700
PMCPMC8248389
OpenAlexW3129038290

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.