Evidence map›Paper›PMID 33028948›Full record

ArticleExperimental & molecular medicine2020

SET8 suppression mediates high glucose-induced vascular endothelial inflammation via the upregulation of PTEN.

Xuefang Shen, Xiangyuan Chen, Jing Wang, Jing Liu, Zhiyao Wang, Qing Hua, Qichao Wu, Yanguang Su, Huanzhong He, Yuqin Hu and 3 more

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

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  15. Methyltransferase SET domain family and its relationship with cardiovascular development and diseases.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022
    Article
  16. Article
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  18. Epigenetics in the pathogenesis of diabetic nephropathy.Acta biochimica et biophysica Sinica · 2022
    Review
  19. 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

13 authors at 4 institutions in 1 country.

Xuefang Shen *Department of Anaesthesiology, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Xiangyuan Chen *Department of Anaesthesiology, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Jing Wang *Department of Anaesthesiology, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Jing Liu *Department of Anaesthesiology, Huzhou Central Hospital, Affiliated Central Hospital of HuZhou University, 313000, Huzhou, Zhejiang, China.
Zhiyao Wang *Department of Anesthesia, Zhongshan Hospital, Fudan University, 200032, Shanghai, China.
Qing HuaDepartment of Anaesthesiology, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Qichao WuDepartment of Anaesthesiology, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Yanguang SuDepartment of Anaesthesiology, Huzhou Maternal & Child Health Care Hospital, 313000, Huzhou, Zhejiang, China.
Huanzhong HeDepartment of Anaesthesiology, Huzhou Maternal & Child Health Care Hospital, 313000, Huzhou, Zhejiang, China.
Yuqin HuDepartment of Anaesthesiology, Huzhou Maternal & Child Health Care Hospital, 313000, Huzhou, Zhejiang, China.
Zhipeng MengDepartment of Anaesthesiology, Huzhou Central Hospital, Affiliated Central Hospital of HuZhou University, 313000, Huzhou, Zhejiang, China. meng_zhipeng@126.com.
Wanxia XiongDepartment of Anesthesia, Zhongshan Hospital, Fudan University, 200032, Shanghai, China. xiong.wanxia@zs-hospital.sh.cn.
Minmin ZhuDepartment of Anaesthesiology, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, 200032, Shanghai, China. zhu_mm@126.com.ORCID http://orcid.org/0000-0002-4951-1421
Fudan University Shanghai Cancer Center · CNHuzhou Women and Children's Hospital · CNHuzhou Central Hospital · CNSun Yat-sen University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81871590
6 · The paper itself

Abstract

Hyperglycemia-mediated endothelial inflammation participates in the pathogenesis of cardiovascular complications in subjects with diabetes. Previous studies reported that phosphatase and tensin homolog deleted on chromosome ten (PTEN) and SET8 participate in high glucose-mediated endothelial inflammation. In this study, we hypothesize that SET8 regulates PTEN expression, thus contributing to high glucose-mediated vascular endothelial inflammation. Our data indicated that plasma soluble intercellular adhesion molecule-1 (sICAM-1) and endothelial selectin (e-selectin) were increased in patients with diabetes and diabetic rats. PTEN expression was augmented in the peripheral blood mononuclear cells of patients with diabetes and in the aortic tissues of diabetic rats. Our in vitro study indicated that high glucose increased monocyte/endothelial adhesion, endothelial adhesion molecule expression and p65 phosphorylation in human umbilical vein endothelial cells (HUVECs). Moreover, high glucose led to endothelial inflammation via upregulation of PTEN. Furthermore, high glucose inhibited SET8 expression and histone H4 lysine 20 methylation (H4K20me1), a downstream target of SET8. SET8 overexpression reversed the effects of high-glucose treatment. shSET8-mediated endothelial inflammation was counteracted by siPTEN. Furthermore, SET8 was found to interact with FOXO1. siFOXO1 attenuated high glucose-mediated endothelial inflammation. FOXO1 overexpression-mediated endothelial inflammation was counteracted by siPTEN. H4K20me1 and FOXO1 were enriched in the PTEN promoter region. shSET8 increased PTEN promoter activity and augmented the positive effect of FOXO1 overexpression on PTEN promoter activity. Our in vivo study indicated that SET8 was downregulated and FOXO1 was upregulated in the peripheral blood mononuclear cells of patients with diabetes and the aortic tissues of diabetic rats. In conclusion, SET8 interacted with FOXO1 to modulate PTEN expression in vascular endothelial cells, thus contributing to hyperglycemia-mediated endothelial inflammation.

Indexed as

AdultAgedAnimalsBiomarkersBlood GlucoseCells, CulturedDiabetes Mellitus, Type 2Endothelium, VascularFemaleForkhead Box Protein O1Gene ExpressionGlucoseHistone-Lysine N-MethyltransferaseHumansHuman Umbilical Vein Endothelial CellsImmunohistochemistryBiomarkersBlood GlucoseForkhead Box Protein O1GlucoseHistone-Lysine N-MethyltransferaseKMT5A protein, humanPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID33028948
PMCPMC8080680
OpenAlexW3092162586

What OpenQuestion holds

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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.