Evidence map›Paper›PMID 26705326›Full record

ArticleRheumatology (Oxford, England)2016

Scleroderma dermal microvascular endothelial cells exhibit defective response to pro-angiogenic chemokines.

Pei-Suen Tsou, Bradley J Rabquer, Ray A Ohara, William A Stinson, Phillip L Campbell, M Asif Amin, Beatrix Balogh, George Zakhem, Paul A Renauer, Ann Lozier and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Rheumatology (Oxford, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Endothelial Dysfunction in Systemic Sclerosis.International journal of molecular sciences · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
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  11. Inhibition of EZH2 prevents fibrosis and restores normal angiogenesis in scleroderma.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. 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

16 authors at 5 institutions in 1 country.

Pei-Suen TsouDivision of Rheumatology, Department of Internal Medicine, University of Michigan Scleroderma Program, ptsou@med.umich.edu.
Bradley J RabquerDivision of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Biology Department, Albion College, Albion, MI.
Ray A OharaDivision of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor.
William A StinsonDivision of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor.
Phillip L CampbellDivision of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor.
M Asif AminDivision of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor.
Beatrix BaloghDivision of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor.
George ZakhemDivision of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor.
Paul A RenauerDivision of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor.
Ann LozierDivision of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor.
Eshwar ArasuDivision of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor.
G Kenneth HainesDepartment of Pathology, Yale University, New Haven, CT.
Bashar KahalehDepartment of Medicine, University of Toledo Medical Center, Toledo, OH and.
Elena SchiopuDivision of Rheumatology, Department of Internal Medicine, University of Michigan Scleroderma Program.
Dinesh KhannaDivision of Rheumatology, Department of Internal Medicine, University of Michigan Scleroderma Program.
Alisa E KochDivision of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, VA Medical Service, Ann Arbor, MI, USA.
University of Michigan–Ann Arbor · USAnn Arbor VA Medical Center · USScleroderma Foundation · USUniversity of Toledo Medical Center · USYale University · US

Funding

TRAINING OF ARTHRITIS RESEARCH SCIENTISTST32AR007080 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Jason Knight · 1986 to 2026
$6.3M
Outcomes Research in Rheumatic DiseasesK24AR063120 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KHANNA, DINESH · 2012 to 2022
$1.6M
NCI NIH HHS CA46952NIAMS NIH HHS 2T32AR007080NIAMS NIH HHS K24 AR063120NIAMS NIH HHS T32 AR007080
6 · The paper itself

Abstract

objectivesAngiogenesis plays a critical role in SSc (scleroderma). The aim of this study was to examine the expression of growth-regulated protein-γ (Gro-γ/CXCL3), granulocyte chemotactic protein 2 (GCP-2/CXCL6) and their receptor CXCR2 in endothelial cells (ECs) isolated from SSc skin and determine whether these cells mount an angiogenic response towards pro-angiogenic chemokines. The downstream signalling pathways as well as the pro-angiogenic transcription factor inhibitor of DNA-binding protein 1 (Id-1) were also examined.

methodsSkin biopsies were obtained from patients with dcSSc. ECs were isolated via magnetic positive selection. Angiogenesis was measured by EC chemotaxis assay.

resultsGro-γ/CXCL3 and GCP-2/CXCL6 were minimally expressed in both skin types but elevated in SSc serum. Pro-angiogenic chemokine mRNA was greater in SSc ECs than in normal ECs. SSc ECs did not migrate to vascular endothelial growth factor (VEGF), Gro-γ/CXCL3, GCP-2/CXCL6 or CXCL16. The signalling pathways stimulated by these chemokines were also dysregulated. Id-1 mRNA in SSc ECs was lower compared with normal ECs, and overexpression of Id-1 in SSc ECs increased their ability to migrate towards VEGF and CXCL16.

conclusionOur results show that SSc ECs are unable to respond to pro-angiogenic chemokines despite their increased expression in serum and ECs. This might be due to the differences in the signalling pathways activated by these chemokines in normal vs SSc ECs. In addition, the lower expression of Id-1 also decreases the angiogenic response. The inability of pro-angiogenic chemokines to promote EC migration provides an additional mechanism for the impaired angiogenesis that characterizes SSc.

Indexed as

Angiogenesis Inducing AgentsCase-Control StudiesCells, CulturedChemokinesChemotaxisEndothelial CellsEndothelium, VascularFemaleHumansInhibitor of Differentiation Protein 1MaleMiddle AgedNeovascularization, PathologicReceptors, Interleukin-8BScleroderma, SystemicSignal TransductionAngiogenesis Inducing AgentsChemokinesID1 protein, humanInhibitor of Differentiation Protein 1phorbolol myristate acetateReceptors, Interleukin-8BTetradecanoylphorbol Acetateangiogenesischemokinesscleroderma

Identifiers

PMID26705326
PMCPMC5009475
OpenAlexW2254661184

What OpenQuestion holds

Textmetadata
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.