Evidence map›Paper›PMID 26733204›Full record

ArticleThe Journal of biological chemistry2016

Interleukin-17A Promotes Aortic Endothelial Cell Activation via Transcriptionally and Post-translationally Activating p38 Mitogen-activated Protein Kinase (MAPK) Pathway.

Jietang Mai, Gayani Nanayakkara, Jahaira Lopez-Pastrana, Xinyuan Li, Ya-Feng Li, Xin Wang, Ai Song, Anthony Virtue, Ying Shao, Huimin Shan and 7 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

78 citing papers in PubMed, 89 citations in OpenAlex.

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  12. Bridging worlds: a narrative review of IL-17 at the crossroads of inflammation and thrombosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  16. Immunomodulation by allograft endothelial cells.Frontiers in transplantation · 2025
    Review
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18 more citing papers are in PubMed but not listed here.

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

17 authors at 3 institutions in 2 countries.

Jietang MaiFrom the Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research and Departments of Pharmacology and.
Gayani NanayakkaraFrom the Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research and.
Jahaira Lopez-PastranaFrom the Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research and.
Xinyuan LiFrom the Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research and Departments of Pharmacology and.
Ya-Feng LiFrom the Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research and.
Xin WangFrom the Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research and.
Ai SongFrom the Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research and.
Anthony VirtueFrom the Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research and Departments of Pharmacology and.
Ying ShaoFrom the Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research and.
Huimin ShanFrom the Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research and.
Fang LiuFrom the Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research and.
Michael V AutieriPhysiology, Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania 19140 and.
Satya P KunapuliFrom the Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research and Physiology, Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania 19140 and.
Yoichiro IwakuraCenter for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan.
Xiaohua JiangFrom the Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research and.
Hong WangFrom the Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research and Departments of Pharmacology and.
Xiao-Feng YangFrom the Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research and Departments of Pharmacology and xfyang@temple.edu.
The Centers · USTemple University · USTokyo University of Science · JP

Funding

miRNA-mediated reduction of VSMC foam cell formationR01HL117724 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI AUTIERI, MICHAEL V · 2013 to 2022
$3.8M
Atherogenic mechanisms with homocysteineR01HL077288 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2004 to 2014
$3.8M
Hyperhomocysteinemia and HDL MetabolismR01HL117654 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2013 to 2017
$3.0M
Caspase-1 activation mediates chronic kidney disease-accelerated atherosclerosisR01HL131460 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI CHOI, ERIC T., WANG, HONG · 2016 to 2019
$2.8M
NADHP Oxidase-mediated MC differentiation & Endothelial Dysfunction in HHcyR01HL110764 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2011 to 2015
$2.5M
IL-35 suppression of endothelial cell activation and atherosclerosisR01HL132399 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2017 to 2020
$2.3M
HHcy-induced Inflammatory Monocyte and Macrophage Differentiation in DiabetesR01DK104116 · NIDDK · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2015 to 2019
$2.2M
Attenuation of atherosclerosis by regulation of VSMC inflammatory gene mRNA stabilityR01HL141108 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI AUTIERI, MICHAEL V · 2018 to 2021
$2.0M
Roles of Interleukin-17 in Endothelial CellsR01HL108910 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2011 to 2015
$1.9M
HHcy-induced Bax upregulation, Treg apoptosis and vascular diseaseR01HL116917 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2013 to 2016
$1.6M
NHLBI NIH HHS 1R01HL131460-01NHLBI NIH HHS 5R01HL077288-11NHLBI NIH HHS 5R01HL108910-05NHLBI NIH HHS 5R01HL110764-05NHLBI NIH HHS 5R01HL116917-03NHLBI NIH HHS 5R01HL117654-03NHLBI NIH HHS R01 HL077288NHLBI NIH HHS R01 HL108910NHLBI NIH HHS R01 HL110764NHLBI NIH HHS R01 HL116917NHLBI NIH HHS R01 HL117654NHLBI NIH HHS R01 HL117724NHLBI NIH HHS R01 HL131460NHLBI NIH HHS R01 HL132399NHLBI NIH HHS R01 HL141108NIDDK NIH HHS 1R01DK104116-01A1NIDDK NIH HHS R01 DK104116
6 · The paper itself

Abstract

Interleukin-17 (IL-17)-secreting T helper 17 cells were recently identified as a CD4(+) T helper subset and implicated in various inflammatory and autoimmune diseases. The issues of whether and by what mechanism hyperlipidemic stress induces IL-17A to activate aortic endothelial cells (ECs) and enhance monocyte adhesion remained largely unknown. Using biochemical, immunological, microarray, experimental data mining analysis, and pathological approaches focused on primary human and mouse aortic ECs (HAECs and MAECs) and our newly generated apolipoprotein E (ApoE)(-/-)/IL-17A(-/-) mice, we report the following new findings. 1) The hyperlipidemia stimulus oxidized low density lipoprotein up-regulated IL-17 receptor(s) in HAECs and MAECs. 2) IL-17A activated HAECs and increased human monocyte adhesion in vitro. 3) A deficiency of IL-17A reduced leukocyte adhesion to endothelium in vivo. 3) IL-17A activated HAECs and MAECs via up-regulation of proinflammatory cytokines IL-6, granulocyte-macrophage colony-stimulating factor (GM-CSF), chemokine CXC motif ligand 1 (CXCL1), and CXCL2. 4) IL-17A activated ECs specifically via the p38 mitogen-activated protein kinases (MAPK) pathway; the inhibition of p38 MAPK in ECs attenuated IL-17A-mediated activation by ameliorating the expression of the aforementioned proinflammatory cytokines, chemokines, and EC adhesion molecules including intercellular adhesion molecule 1. Taken together, our results demonstrate for the first time that IL-17A activates aortic ECs specifically via p38 MAPK pathway.

Indexed as

MAP Kinase Signaling SystemAnimalsAortaApolipoproteins ECell AdhesionCells, CulturedChemokine CXCL1Endothelial CellsGranulocyte-Macrophage Colony-Stimulating FactorHumansHyperlipidemiasInterleukin-17Interleukin-6MiceMice, Inbred C57BLMonocytesApolipoproteins EChemokine CXCL1Granulocyte-Macrophage Colony-Stimulating FactorIl17a protein, mouseInterleukin-17Interleukin-6p38 Mitogen-Activated Protein KinasesReceptors, Interleukin-17cardiovascular diseaseendothelial cellendothelial cell activationinflammationinterleukin 17A (IL-17 or IL-17A)monocyte adhesionp38 MAPK

Identifiers

PMID26733204
PMCPMC4777832
OpenAlexW2294519835

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.