Evidence map›Paper›PMID 26293469›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2015

Post-Transcriptional Regulation of Endothelial Nitric Oxide Synthase Expression by Polypyrimidine Tract-Binding Protein 1.

Bing Yi, Maria Ozerova, Guan-Xin Zhang, Guijun Yan, Shengdong Huang, Jianxin Sun

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
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  5. Gangliosides Contribute to Vascular Insulin Resistance.International journal of molecular sciences · 2019
    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 at 2 institutions in 2 countries.

Bing YiFrom the Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, PA (B.Y., M.O., J.S.); Reproductive Medicine Center, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China (G.Y.); and Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China (G.Z., S.H., J.S.).
Maria OzerovaFrom the Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, PA (B.Y., M.O., J.S.); Reproductive Medicine Center, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China (G.Y.); and Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China (G.Z., S.H., J.S.).
Guan-Xin ZhangFrom the Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, PA (B.Y., M.O., J.S.); Reproductive Medicine Center, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China (G.Y.); and Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China (G.Z., S.H., J.S.).
Guijun YanFrom the Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, PA (B.Y., M.O., J.S.); Reproductive Medicine Center, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China (G.Y.); and Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China (G.Z., S.H., J.S.).
Shengdong HuangFrom the Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, PA (B.Y., M.O., J.S.); Reproductive Medicine Center, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China (G.Y.); and Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China (G.Z., S.H., J.S.).
Jianxin SunFrom the Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, PA (B.Y., M.O., J.S.); Reproductive Medicine Center, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China (G.Y.); and Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China (G.Z., S.H., J.S.). jianxin.sun@jefferson.edu.
Nanjing Drum Tower Hospital · CNThomas Jefferson University · US

Funding

Regulation of Endothelial Nitric Oxide Synthase mRNA StabilityR01HL103869 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SUN, JIANXIN · 2010 to 2020
$3.5M
NHLBI NIH HHS HL103869NHLBI NIH HHS R01 HL103869
6 · The paper itself

Abstract

objectiveEndothelial nitric oxide synthase (eNOS) is an important regulator of vascular function and its expression is regulated at post-transcriptional levels through a yet unknown mechanism. The purpose of this study is to elucidate the post-transcriptional factors regulating eNOS expression and function in endothelium. APPROACHES AND

resultsTo elucidate the molecular basis of tumor necrosis factor (TNF)-α-mediated eNOS mRNA instability, biotinylated eNOS 3'-untranslational region (UTR) was used to purify its associated proteins by RNA affinity chromatography from cytosolic fractions of TNF-α-stimulated human umbilical vein endothelial cells (HUVECs). We identified 2 cytosolic proteins, with molecular weight of 52 and 57 kDa, which specifically bind to eNOS 3'-UTR in response to TNF-α stimulation. Matrix-assisted laser desorption ionization time-of-flight mass spectrometric analysis identified the 57-kDa protein as polypyrimidine tract-binding protein 1 (PTB1). RNA gel mobility shift and UV cross-linking assays demonstrated that PTB1 binds to a UCUU-rich sequence in eNOS 3'-UTR, and the C-terminal half of PTB1 is critical to this interaction. Importantly, PTB1 overexpression leads to decreased activity of luciferase gene fused with eNOS 3'-UTR as well as reduced eNOS expression and activity in human ECs. In HUVECs, we show that TNF-α markedly increased PTB1 expression, whereas adenovirus-mediated PTB1 overexpression decreased eNOS mRNA stability and reduced protein expression and endothelium-dependent relaxation. Furthermore, knockdown of PTB1 substantially attenuated TNF-α-induced destabilization of eNOS transcript and downregulation of eNOS expression.

conclusionsThese results indicate that PTB1 is essential for regulating eNOS expression at post-transcriptional levels and suggest a novel therapeutic target for treatment of vascular diseases associated with inflammatory endothelial dysfunction.

Indexed as

Gene Expression RegulationCells, CulturedDown-RegulationEndothelium, VascularHumansHuman Umbilical Vein Endothelial CellsNitric Oxide Synthase Type IIIPolypyrimidine Tract-Binding ProteinProtein BindingRNA, MessengerRNA StabilitySensitivity and SpecificityTranscription FactorsTumor Necrosis Factor-alphaNitric Oxide Synthase Type IIINOS3 protein, humanPolypyrimidine Tract-Binding ProteinRNA, MessengerTNF protein, humanTranscription FactorsTumor Necrosis Factor-alphaendotheliumluciferaseRNA stabilitytumor necrosis factor-αvascular diseases

Identifiers

PMID26293469
PMCPMC6027644
OpenAlexW2129809626

What OpenQuestion holds

Textmetadata
LicenceTDM
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.