Evidence map›Paper›PMID 29394092›Full record

ArticleAmerican journal of respiratory cell and molecular biology2018

Deficient Follistatin-like 3 Secretion by Asthmatic Airway Epithelium Impairs Fibroblast Regulation and Fibroblast-to-Myofibroblast Transition.

Richard G James, Stephen R Reeves, Kaitlyn A Barrow, Maria P White, Veronika A Glukhova, Candace Haghighi, Dana Seyoum, Jason S Debley

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 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Optimized primary organotypic culture from murine neonatal tracheal airway epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2026
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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

8 authors at 1 institution in 1 country.

Richard G James1 Department of Pediatrics.
Stephen R Reeves4 Division of Pulmonary Medicine, Seattle Children's Hospital, University of Washington, Seattle, Washington; and.
Kaitlyn A Barrow3 Center for Immunity and Immunotherapies, Seattle Children's Research Institute, Seattle, Washington.
Maria P White3 Center for Immunity and Immunotherapies, Seattle Children's Research Institute, Seattle, Washington.
Veronika A Glukhova3 Center for Immunity and Immunotherapies, Seattle Children's Research Institute, Seattle, Washington.
Candace Haghighi3 Center for Immunity and Immunotherapies, Seattle Children's Research Institute, Seattle, Washington.
Dana Seyoum3 Center for Immunity and Immunotherapies, Seattle Children's Research Institute, Seattle, Washington.
Jason S Debley4 Division of Pulmonary Medicine, Seattle Children's Hospital, University of Washington, Seattle, Washington; and.ORCID 0000-0001-6438-9535
Seattle Children's Hospital · US

Funding

Dysregulated Airway Epithelial Signaling as a Driver of Airway Remodeling in Asthmatic ChildrenR01HL128361 · NHLBI · SEATTLE CHILDREN'S HOSPITAL · PI DEBLEY, JASON S · 2016 to 2018
$1.4M
In vivo role of BTK-mediated inhibition of Wnt/b-catenin signaling during hematopR00HL103768 · NHLBI · SEATTLE CHILDREN'S HOSPITAL · PI JAMES, RICHARD GOFF · 2012 to 2014
$717k
NHLBI NIH HHS R00 HL103768NHLBI NIH HHS R01 HL128361
6 · The paper itself

Abstract

Bronchial epithelial cells (BECs) from healthy children inhibit human lung fibroblast (HLF) expression of collagen and fibroblast-to-myofibroblast transition (FMT), whereas asthmatic BECs do so less effectively, suggesting that diminished epithelial-derived regulatory factors contribute to airway remodeling. Preliminary data demonstrated that secretion of the activin A inhibitor follistatin-like 3 (FSTL3) by healthy BECs was greater than that by asthmatic BECs. We sought to determine the relative secretion of FSTL3 and activin A by asthmatic and healthy BECs, and whether FSTL3 inhibits FMT. To quantify the abundance of the total proteome FSTL3 and activin A in supernatants of differentiated BEC cultures from healthy children and children with asthma, we performed mass spectrometry and ELISA. HLFs were cocultured with primary BECs and then HLF expression of collagen I and α-smooth muscle actin (α-SMA) was quantified by qPCR, and FMT was quantified by flow cytometry. Loss-of-function studies were conducted using lentivirus-delivered shRNA. Using mass spectrometry and ELISA results from larger cohorts, we found that FSTL3 concentrations were greater in media conditioned by healthy BECs compared with asthmatic BECs (4,012 vs. 2,553 pg/ml; P = 0.002), and in media conditioned by asthmatic BECs from children with normal lung function relative to those with airflow obstruction (FEV

Indexed as

ActinsActivinsAdolescentAmino Acid SequenceAsthmaChildCollagen Type IEpithelial CellsEpitheliumFemaleFollistatin-Related ProteinsGene Knockdown TechniquesHumansLungMaleMyofibroblastsACTA2 protein, humanActinsactivin AActivinsCollagen Type IFollistatin-Related ProteinsFstl3 protein, humanRNA, Small Interferingactivin Aairway remodelingasthmaepithelial cellsFSTL3

Identifiers

PMID29394092
PMCPMC6039878
OpenAlexW2791020242

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.