Evidence map›Paper›PMID 26287404›Full record

ArticleEndocrinology2015

Pentraxin-3 Is a TSH-Inducible Protein in Human Fibrocytes and Orbital Fibroblasts.

Hao Wang, Stephen J Atkins, Roshini Fernando, Rui-Li Wei, Terry J Smith

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. 2021 update on thyroid-associated ophthalmopathy.Journal of endocrinological investigation · 2022
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. IGF1 receptor and thyroid-associated ophthalmopathy.Journal of molecular endocrinology · 2018
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 2 institutions in 2 countries.

Hao WangDepartments of Ophthalmology and Visual Sciences (H.W., S.J.A., R.F., T.J.S.), University of Michigan Medical School, Ann Arbor, Michigan 48105; Department of Ophthalmology (H.W., R.-L.W.), Shanghai Changzheng Hospital, Second Military Medical University, 200003 Shanghai, China; and Division of Metabolism (T.J.S.), Endocrinology, and Diabetes, University of Michigan Medical School, Ann Arbor, Michigan 48105.
Stephen J AtkinsDepartments of Ophthalmology and Visual Sciences (H.W., S.J.A., R.F., T.J.S.), University of Michigan Medical School, Ann Arbor, Michigan 48105; Department of Ophthalmology (H.W., R.-L.W.), Shanghai Changzheng Hospital, Second Military Medical University, 200003 Shanghai, China; and Division of Metabolism (T.J.S.), Endocrinology, and Diabetes, University of Michigan Medical School, Ann Arbor, Michigan 48105.
Roshini FernandoDepartments of Ophthalmology and Visual Sciences (H.W., S.J.A., R.F., T.J.S.), University of Michigan Medical School, Ann Arbor, Michigan 48105; Department of Ophthalmology (H.W., R.-L.W.), Shanghai Changzheng Hospital, Second Military Medical University, 200003 Shanghai, China; and Division of Metabolism (T.J.S.), Endocrinology, and Diabetes, University of Michigan Medical School, Ann Arbor, Michigan 48105.
Rui-Li WeiDepartments of Ophthalmology and Visual Sciences (H.W., S.J.A., R.F., T.J.S.), University of Michigan Medical School, Ann Arbor, Michigan 48105; Department of Ophthalmology (H.W., R.-L.W.), Shanghai Changzheng Hospital, Second Military Medical University, 200003 Shanghai, China; and Division of Metabolism (T.J.S.), Endocrinology, and Diabetes, University of Michigan Medical School, Ann Arbor, Michigan 48105.
Terry J SmithDepartments of Ophthalmology and Visual Sciences (H.W., S.J.A., R.F., T.J.S.), University of Michigan Medical School, Ann Arbor, Michigan 48105; Department of Ophthalmology (H.W., R.-L.W.), Shanghai Changzheng Hospital, Second Military Medical University, 200003 Shanghai, China; and Division of Metabolism (T.J.S.), Endocrinology, and Diabetes, University of Michigan Medical School, Ann Arbor, Michigan 48105.
University of Michigan–Ann Arbor · USSecond Military Medical University · CN

Funding

VIVARIUM MODULEP30EY007003 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI David Antonetti · 1987 to 2026
$17.6M
REGULATION OF RETROOCULAR CONNECTIVE TISSUER01EY008976 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SMITH, TERRY J · 1993 to 2020
$6.4M
E75 IN THE DEVELOPING DROSOPHILA EYEF31EY007003 · NEI · YALE UNIVERSITY · PI SHILTON, ALYCIA N · 1999 to 2001
$14k
NEI NIH HHS EY007003NEI NIH HHS EY008976NEI NIH HHS F31 EY007003NEI NIH HHS P30 EY007003NEI NIH HHS R01 EY008976
6 · The paper itself

Abstract

CD34(+) fibrocytes are bone marrow-derived monocyte progenitor cells that traffic to sites of tissue injury and repair. They putatively infiltrate the orbit in thyroid-associated ophthalmopathy where they appear to transition into CD34(+) orbital fibroblasts (OFs) that interact with residential CD34(-) fibroblasts. A unique phenotypic attribute of fibrocytes and CD34(+) OFs is their expression of the functional thyrotropin receptor (TSHR) and other "thyroid-specific" proteins. When activated through TSHR, fibrocytes express a number of cytokines and other inflammatory genes. Here we sought to determine whether pentraxin-3 (PTX-3), an acute-phase protein involved in inflammation and autoimmunity, might be induced by TSH in fibrocytes and OFs. These cells were collected from patients with Graves disease and healthy individuals. PTX-3 mRNA levels were determined by real-time PCR, protein was determined by ELISA and Western blot, and PTX-3 gene promoter activity was assessed with reporter assays. PTX-3 expression was induced by TSH in both cell types, regardless of the health status of the donor and was a consequence of increased steady-state PTX-3 mRNA levels. M22, a TSHR-activating monoclonal antibody, also induced PTX-3. The induction could be attenuated by dexamethasone and by IGF-I receptor-blocking antibodies, teprotumumab and 1H7. TSH effects were mediated through phosphatidylinositol 3-kinase/AKT, mammalian target of rapamycin/p70(s6k), Janus tyrosine kinase 2 pathways, and enhanced PTX-3 mRNA stability. These findings indicate that PTX-3 is a TSH target gene, the expression of which can be induced in fibrocytes and OFs. They suggest that PTX-3 might represent a previously unidentified nexus between the thyroid axis and the mechanisms involved in tissue remodeling.

Indexed as

Bone Marrow CellsCells, CulturedC-Reactive ProteinDexamethasoneFemaleFibroblastsGlucocorticoidsGraves OphthalmopathyHumansMalePentraxinsPromoter Regions, GeneticReceptors, ThyrotropinSerum Amyloid P-ComponentSignal TransductionThyrotropinC-Reactive ProteinDexamethasoneGlucocorticoidsPentraxinsReceptors, ThyrotropinSerum Amyloid P-ComponentThyrotropin

Identifiers

PMID26287404
PMCPMC4606754
OpenAlexW1778701518

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.