Evidence map›Paper›PMID 28886261›Full record

ArticleAmerican journal of respiratory cell and molecular biology2018

Syndecan-2 Attenuates Radiation-induced Pulmonary Fibrosis and Inhibits Fibroblast Activation by Regulating PI3K/Akt/ROCK Pathway via CD148.

Konstantin Tsoyi, Sarah G Chu, Nasly G Patino-Jaramillo, Julie Wilder, Julian Villalba, Melanie Doyle-Eisele, Jacob McDonald, Xiaoli Liu, Souheil El-Chemaly, Mark A Perrella and 1 more

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 75 citations in OpenAlex.

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  18. Identifying Active Substances and the Pharmacological Mechanism ofEvidence-based complementary and alternative medicine : eCAM · 2022
    Article
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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

11 authors at 3 institutions in 1 country.

Konstantin Tsoyi1 Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; and.
Sarah G Chu1 Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; and.
Nasly G Patino-Jaramillo2 Pulmonary Fibrosis Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico.
Julie Wilder2 Pulmonary Fibrosis Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico.
Julian Villalba1 Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; and.
Melanie Doyle-Eisele2 Pulmonary Fibrosis Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico.
Jacob McDonald2 Pulmonary Fibrosis Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico.
Xiaoli Liu1 Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; and.
Souheil El-Chemaly1 Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; and.
Mark A Perrella1 Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; and.
Ivan O Rosas1 Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; and.
Brigham and Women's Hospital · USLovelace Respiratory Research Institute · USHarvard University · US

Funding

Respiratory Computational Discovery CoreP01HL114501 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHOI, MARY E · 2013 to 2025
$24.9M
RESPIRATORY RESEARCHT32HL007633 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI George R Washko · 1985 to 2026
$14.9M
Lymphatics and Lung Allograft RejectionR01HL130275 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI EL-CHEMALY, SOUHEIL · 2016 to 2020
$2.2M
NHLBI NIH HHS P01 HL114501NHLBI NIH HHS R01 HL130275NHLBI NIH HHS T32 HL007633
6 · The paper itself

Abstract

Radiation-induced pulmonary fibrosis is a severe complication of patients treated with thoracic irradiation. We have previously shown that syndecan-2 reduces fibrosis by exerting alveolar epithelial cytoprotective effects. Here, we investigate whether syndecan-2 attenuates radiation-induced pulmonary fibrosis by inhibiting fibroblast activation. C57BL/6 wild-type mice and transgenic mice that overexpress human syndecan-2 in alveolar macrophages were exposed to 14 Gy whole-thoracic radiation. At 24 weeks after irradiation, lungs were collected for histological, protein, and mRNA evaluation of pulmonary fibrosis, profibrotic gene expression, and α-smooth muscle actin (α-SMA) expression. Mouse lung fibroblasts were activated with transforming growth factor (TGF)-β1 in the presence or absence of syndecan-2. Cell proliferation, migration, and gel contraction were assessed at different time points. Irradiation resulted in significantly increased mortality and pulmonary fibrosis in wild-type mice that was associated with elevated lung expression of TGF-β1 downstream target genes and cell death compared with irradiated syndecan-2 transgenic mice. In mouse lung fibroblasts, syndecan-2 inhibited α-SMA expression, cell contraction, proliferation, and migration induced by TGF-β1. Syndecan-2 attenuated phosphoinositide 3-kinase/serine/threonine kinase/Rho-associated coiled-coil kinase signaling and serum response factor binding to the α-SMA promoter. Syndecan-2 attenuates pulmonary fibrosis in mice exposed to radiation and inhibits TGF-β1-induced fibroblast-myofibroblast differentiation, migration, and proliferation by down-regulating phosphoinositide 3-kinase/serine/threonine kinase/Rho-associated coiled-coil kinase signaling and blocking serum response factor binding to the α-SMA promoter via CD148. These findings suggest that syndecan-2 has potential as an antifibrotic therapy in radiation-induced lung fibrosis.

Indexed as

AnimalsCell MovementCell ProliferationFemaleMiceMice, Inbred C57BLMice, TransgenicMyofibroblastsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPulmonary FibrosisRadiation InjuriesReceptor-Like Protein Tyrosine Phosphatases, Class 3rho-Associated KinasesSyndecan-2ThoraxPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPtprj protein, mouseReceptor-Like Protein Tyrosine Phosphatases, Class 3rho-Associated KinasesRock1 protein, mouseSDC2 protein, humanSyndecan-2Transforming Growth Factor betafibroblastmyofibroblastpulmonary fibrosisradiationsyndecan-2

Identifiers

PMID28886261
PMCPMC5805997
OpenAlexW2753275287

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.