Evidence map›Paper›PMID 27597766›Full record

ArticlePhysiological reports2016

CRISPLD2 (LGL1) inhibits proinflammatory mediators in human fetal, adult, and COPD lung fibroblasts and epithelial cells.

Hui Zhang, Alvin T Kho, Qing Wu, Andrew J Halayko, Karen Limbert Rempel, Robert P Chase, Neil B Sweezey, Scott T Weiss, Feige Kaplan

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
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  7. Article
  8. Article
  9. CAP superfamily proteins in human: a new target for cancer therapy.Medical oncology (Northwood, London, England) · 2024
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  17. Matters of the heart: Cellular sex differences.Journal of molecular and cellular cardiology · 2021
    Review
  18. Article
  19. In vitro and bioinformatics mechanistic-based approach for cadmium carcinogenicity understanding.Toxicology in vitro : an international journal published in association with BIBRA · 2020
    Article
  20. Pharmacogenetics of Pediatric Asthma: Current Perspectives.Pharmacogenomics and personalized medicine · 2020
    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

9 authors at 6 institutions in 2 countries.

Hui ZhangResearch Institute of the McGill University Health Centre, Montreal, Quebec, Canada.
Alvin T KhoChildren's Hospital Informatics Program Boston Children's Hospital, Boston, Massachusetts.
Qing WuResearch Institute of the McGill University Health Centre, Montreal, Quebec, Canada.
Andrew J HalaykoDepartment of Physiology and Pathophysiology, University of Manitoba, Winnipeg, Manitoba, Canada Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada Biology of Breathing Group, Manitoba Institute of Child Health, Winnipeg, Manitoba, Canada.
Karen Limbert RempelDepartment of Physiology and Pathophysiology, University of Manitoba, Winnipeg, Manitoba, Canada Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada Biology of Breathing Group, Manitoba Institute of Child Health, Winnipeg, Manitoba, Canada.
Robert P ChaseChanning Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital Harvard Medical School, Boston, Massachusetts.
Neil B SweezeyThe Hospital for Sick Children Research Institute, Toronto, Ontario, Canada Departments of Paediatrics and Physiology, University of Toronto, Toronto, Ontario, Canada.
Scott T WeissChanning Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital Harvard Medical School, Boston, Massachusetts.
Feige KaplanResearch Institute of the McGill University Health Centre, Montreal, Quebec, Canada Departments of Human Genetics and Pediatrics, McGill University, Montreal, Quebec, Canada feige.kaplan@mcgill.ca.
McGill University Health Centre · CAHarvard University · USBoston Children's Hospital · USChildren's Hospital Research Institute of Manitoba · CAResearch Manitoba · CAUniversity of Toronto · CA

Funding

INTRAUTERINE SMOKE EXPOSURE AND ASTHMA: GENOMIC ORIGINSR01HL097144 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI KOBZIK, LESTER, WEISS, SCOTT T · 2009 to 2013
$2.9M
A Developmental Basis for Chronic Obstructive Lung DiseaseK25HL091124 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI KHO, ALVIN THONG-JUAK · 2008 to 2012
$743k
NHLBI NIH HHS K25 HL091124NHLBI NIH HHS R01 HL097144
6 · The paper itself

Abstract

Chronic lung disease of prematurity/bronchopulmonary dysplasia (BPD) is the leading cause of perinatal morbidity in developed countries. Inflammation is a prominent finding. Currently available interventions have associated toxicities and limited efficacy. While BPD often resolves in childhood, survivors of preterm birth are at risk for acquired respiratory disease in early life and are more likely to develop chronic obstructive pulmonary disease (COPD) in adulthood. We previously cloned Crispld2 (Lgl1), a glucocorticoid-regulated mesenchymal secretory protein that modulates lung branching and alveogenesis through mesenchymal-epithelial interactions. Absence of Crispld2 is embryonic lethal. Heterozygous Crispld2+/- mice display features of BPD, including distal airspace enlargement, disruption of elastin, and neonatal lung inflammation. CRISPLD2 also plays a role in human fetal lung fibroblast cell expansion, migration, and mesenchymal-epithelial signaling. This study assessed the effects of endogenous and exogenous CRISPLD2 on expression of proinflammatory mediators in human fetal and adult (normal and COPD) lung fibroblasts and epithelial cells. CRISPLD2 expression was upregulated in a lipopolysaccharide (LPS)-induced human fetal lung fibroblast line (MRC5). LPS-induced upregulation of the proinflammatory cytokines IL-8 and CCL2 was exacerbated in MRC5-CRISPLD2(knockdown) cells. siRNA suppression of endogenous CRISPLD2 in adult lung fibroblasts (HLFs) led to augmented expression of IL-8, IL-6, CCL2. LPS-stimulated expression of proinflammatory mediators by human lung epithelial HAEo- cells was attenuated by purified secretory CRISPLD2. RNA sequencing results from HLF-CRISPLD2(knockdown) suggest roles for CRISPLD2 in extracellular matrix and in inflammation. Our data suggest that suppression of CRISPLD2 increases the risk of lung inflammation in early life and adulthood.

Indexed as

AdultAgedAnimalsBronchopulmonary DysplasiaCell Adhesion MoleculesCell ProliferationCells, CulturedEpithelial CellsEpithelial-Mesenchymal TransitionFibroblastsHEK293 CellsHumansInflammation MediatorsInterferon Regulatory FactorsInterleukin-6LipopolysaccharidesCell Adhesion MoleculesCRISPLD2 protein, humanInflammation MediatorsInterferon Regulatory FactorsInterleukin-6LipopolysaccharidesBronchopulmonary dysplasia (BPD)CRISPLD2 (LGL1)human fetal/adult lung fibroblastmesenchymal–epithelial interactionpro/antiinflammation

Identifiers

PMID27597766
PMCPMC5027350
OpenAlexW2511326256

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.