Evidence map›Paper›PMID 29180197›Full record

ArticleThe Journal of surgical research2017

TSG-6 is highly expressed in human abdominal aortic aneurysms.

S Keisin Wang, Jie Xie, Linden A Green, Robert A McCready, Raghu L Motaganahalli, Andres Fajardo, Clifford C Babbey, Michael P Murphy

Open access · greenAbstract read
In one paragraph

Article in The Journal of surgical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. Knockdown of lncRNAMolecules and cells · 2019
    Article
  4. Article
  5. Review
  6. Review
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 1 country.

S Keisin WangIndiana University School of Medicine, Richard Roudebush Veteran Affairs Medical Center, Department of Surgery, Division of Vascular Surgery and Center for Aortic Disease, Indianapolis, Indiana.
Jie XieIndiana University School of Medicine, Richard Roudebush Veteran Affairs Medical Center, Department of Surgery, Division of Vascular Surgery and Center for Aortic Disease, Indianapolis, Indiana.
Linden A GreenIndiana University School of Medicine, Richard Roudebush Veteran Affairs Medical Center, Department of Surgery, Division of Vascular Surgery and Center for Aortic Disease, Indianapolis, Indiana.
Robert A McCreadyIndiana University School of Medicine, Richard Roudebush Veteran Affairs Medical Center, Department of Surgery, Division of Vascular Surgery and Center for Aortic Disease, Indianapolis, Indiana.
Raghu L MotaganahalliIndiana University School of Medicine, Richard Roudebush Veteran Affairs Medical Center, Department of Surgery, Division of Vascular Surgery and Center for Aortic Disease, Indianapolis, Indiana.
Andres FajardoIndiana University School of Medicine, Richard Roudebush Veteran Affairs Medical Center, Department of Surgery, Division of Vascular Surgery and Center for Aortic Disease, Indianapolis, Indiana.
Clifford C BabbeyIndiana University School of Medicine, Richard Roudebush Veteran Affairs Medical Center, Department of Surgery, Division of Vascular Surgery and Center for Aortic Disease, Indianapolis, Indiana.
Michael P MurphyIndiana University School of Medicine, Richard Roudebush Veteran Affairs Medical Center, Department of Surgery, Division of Vascular Surgery and Center for Aortic Disease, Indianapolis, Indiana. Electronic address: mipmurph@iupui.edu.
Richard L. Roudebush VA Medical Center · US

Funding

Utility of Autologous and Allogeneic Cell Therapy for Peripheral Arterial DiseaseUM1HL113457 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI MURPHY, MICHAEL PATRICK · 2012 to 2018
$3.0M
A Clinical and Histological Analysis of Mesenchymal Stem Cells in AmputationR01HL128827 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI MURPHY, MICHAEL PATRICK · 2016 to 2019
$1.8M
Mesenchymal stem cells induce regulatory T cells in patients with aortic aneurysmI01CX001407 · VA · RLR VA MEDICAL CENTER · PI MURPHY, MICHAEL PATRICK · 2017 to 2021
–
CSRD VA I01 CX001407NHLBI NIH HHS R01 HL128827NHLBI NIH HHS UM1 HL113457
6 · The paper itself

Abstract

backgroundThe formation of abdominal aortic aneurysms (AAA) is characterized by a dominance of proinflammatory forces that result in smooth muscle cell apoptosis, extracellular matrix degradation, and progressive diameter expansion. Additional defects in the antiinflammatory response may also play a role but have yet to be fully characterized. TSG-6 (TNF-stimulated gene-6) is a potent antiinflammatory protein involved in extracellular matrix stabilization and cell migration active in many pathological conditions. Here, we describe its role in AAA formation.

methodsBlood and/or aortic tissue samples were collected from organ donors, subjects undergoing elective AAA screening, and open surgical AAA repair. Aortic specimens collected were preserved for IHC or immediately assayed after tissue homogenization. Protein concentrations in tissue and plasma were assayed by ELISA. All immune cell populations were assayed using FACS. In vitro, macrophage polarization from monocytes was performed with young, healthy donor PBMCs.

resultsTSG-6 was found to be abnormally elevated in both the plasma and aortic wall of patients with AAA compared with healthy and risk-factor matched non-AAA donors. We observed the highest tissue concentration of TSG-6 in the less-diseased proximal and distal shoulders compared with the central aspect of the aneurysm. IHC localized most TSG-6 to the tunica media with minor expression in the tunica adventitia of the aortic wall. Higher concentrations of both M1 and M2 macrophages where also observed, however M1/M2 ratios were unchanged from healthy controls. We observed no difference in M1/M2 ratios in the peripheral blood of risk-factor matched non-AAA and AAA patients. Interesting, TSG-6 inhibited the polarization of the antiinflammatory M2 phenotype in vitro.

conclusionsAAA formation results from an imbalance of inflammatory forces causing aortic wall infiltration of mononuclear cells leading to the vessel breakdown. In the AAA condition, we report an elevation of TSG-6 expression in both the aortic wall and the peripheral circulation.

Indexed as

AgedAorta, AbdominalAortic Aneurysm, AbdominalCase-Control StudiesCell Adhesion MoleculesHumansMacrophagesMaleMuscle, Smooth, VascularCell Adhesion MoleculesTNFAIP6 protein, humanAbdominal aortic aneurysmInflammationMacrophageTSG-6

Identifiers

PMID29180197
PMCPMC5864112
OpenAlexW2746841216

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.