Evidence map›Paper›PMID 30391133›Full record

ArticleMicrovascular research2019

Orphan nuclear receptor TR3/Nur77 differentially regulates the expression of integrins in angiogenesis.

Taiyang Ye, Jin Peng, Xin Liu, Shiqiang Hou, Gengming Niu, Yan Li, Huiyan Zeng, Dezheng Zhao

Abstract read
In one paragraph

Article in Microvascular research, 2019. 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 26% 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, 27 citations in OpenAlex.

  1. Article
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  6. Controversy and multiple roles of the solitary nucleus receptor Nur77 in disease and physiology.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
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  14. TProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  15. Article
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

8 authors at 1 institution in 2 countries.

Taiyang YeCenter for Vascular Biology Research and Division of Gastroenterology, Departments of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA; Department of Obstetrics & Gynecology, Renji Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200127, PR China.
Jin PengCenter for Vascular Biology Research and Division of Gastroenterology, Departments of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA; Radiotherapy and Medical Oncology Department, Zhongnan Hospital, Wuhan University, Wuhan, PR China.
Xin LiuCenter for Vascular Biology Research and Division of Gastroenterology, Departments of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA; Beijing Traditional Chinese Medicine Hospital, Capital Medical University, Beijing, PR China.
Shiqiang HouCenter for Vascular Biology Research and Division of Gastroenterology, Departments of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA; Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, PR China.
Gengming NiuCenter for Vascular Biology Research and Division of Gastroenterology, Departments of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA; Department of General Surgery, Huashan Hospital, Fudan University, Shanghai 200040, PR China.
Yan LiCenter for Vascular Biology Research and Division of Gastroenterology, Departments of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA; Department of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, PR China.
Huiyan ZengCenter for Vascular Biology Research and Division of Gastroenterology, Departments of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA. Electronic address: hzeng@bidmc.harvard.edu.
Dezheng ZhaoCenter for Vascular Biology Research and Division of Gastroenterology, Departments of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA. Electronic address: dzhao@bidmc.harvard.edu.
Beth Israel Deaconess Medical Center · US

Funding

Regulation of colitis by orphan nuclear receptor Nur77R01DK095873 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZHAO, DEZHENG · 2013 to 2017
$1.9M
Orphan Nuclear Receptor TR3 in tumor angiogenesis and associated microvessel permR01CA133235 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZENG, HUIYAN · 2009 to 2013
$1.7M
Orphan nuclear receptor Nur77 and intestinal inflammmationR21DK080970 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZHAO, DEZHENG · 2009 to 2010
$468k
Targeting orphan nuclear receptor TR3/Nur77 for tumor angiogenesisR03CA191463 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZENG, HUIYAN · 2015 to 2016
$174k
Down Syndrome Candidate Region 1 isoform 1L in tumor growth and metastasisR03CA194795 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZENG, HUIYAN · 2015 to 2016
$174k
NCI NIH HHS R01 CA133235NCI NIH HHS R03 CA191463NCI NIH HHS R03 CA194795NIDDK NIH HHS R01 DK095873NIDDK NIH HHS R21 DK080970
6 · The paper itself

Abstract

Pathological angiogenesis is a hallmark of many diseases. Previously, we reported that orphan nuclear receptor TR3/Nur77 (human homolog, Nur77, mouse homolog) is a critical mediator of angiogenesis to regulate tumor growth and skin wound healing via down-regulating the expression of the junctional proteins and integrin β4. However, the molecular mechanism, by which TR3/Nur77 regulated angiogenesis, was still not completely understood. In this report by analyzing the integrin expression profile in endothelial cells, we found that the TR3/Nur77 expression highly increased the expression of integrins α1 and β5, decreased the expression of integrins α2 and β3, but had some or no effect on the expression of integrins αv, α3, α4, α5, α6, β1 and β7. In the angiogenic responses mediated by TR3/Nur77, integrin α1 regulated endothelial cell proliferation and adhesion, but not migration. Integrin β5 shRNA inhibited cell migration, but increased proliferation and adhesion. Integrin α2 regulated all of the endothelial cell proliferation, migration and adhesion. However, integrin β3 did not play any role in endothelial cell proliferation, migration and adhesion. TR3/Nur77 regulated the transcription of integrins α1, α2, β3 and β5, via various amino acid fragments within its transactivation domain and DNA binding domain. Furthermore, TR3/Nur77 regulated the integrin α1 promoter activity by directly interacting with a novel DNA element within the integrin α1 promoter. These studies furthered our understanding of the molecular mechanism by which TR3/Nur77 regulated angiogenesis, and supported our previous finding that TR3/Nur77 was an excellent therapeutic target for pathological angiogenesis. Therefore, targeting TR3/Nur77 inhibits several signaling pathways that are activated by various angiogenic factors.

Indexed as

Neovascularization, PhysiologicAngiogenesis Inducing AgentsBinding SitesCell AdhesionCell MovementCell ProliferationCells, CulturedEndothelial CellsHumansHuman Umbilical Vein Endothelial CellsIntegrinsMicrovesselsNuclear Receptor Subfamily 4, Group A, Member 1Promoter Regions, GeneticSignal TransductionSkinAngiogenesis Inducing AgentsIntegrinsNR4A1 protein, humanNuclear Receptor Subfamily 4, Group A, Member 1Vascular Endothelial Growth Factor AVEGFA protein, humanAngiogenesisIntegrinMigrationProliferationPromoterTR3/Nur77

Identifiers

PMID30391133
PMCPMC6294663
OpenAlexW2899440084

What OpenQuestion holds

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Read underepoch 390

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.