Evidence map›Paper›PMID 34367191›Full record

ArticleFrontiers in immunology2021

Extracellular CIRP Induces an Inflammatory Phenotype in Pulmonary Fibroblasts

Siavash Bolourani, Ezgi Sari, Max Brenner, Ping Wang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Observational
  12. Article
  13. Review
  14. Plasticity towards Rigidity: A Macrophage Conundrum in Pulmonary Fibrosis.International journal of molecular sciences · 2022
    Review
  15. The role of Cold-Inducible RNA-binding protein in respiratory diseases.Journal of cellular and molecular medicine · 2022
    Review
  16. Article
  17. Observational
  18. 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

4 authors at 3 institutions in 1 country.

Siavash BolouraniCenter for Immunology and Inflammation, Feinstein Institutes for Medical Research, Manhasset, NY, United States.
Ezgi SariCenter for Immunology and Inflammation, Feinstein Institutes for Medical Research, Manhasset, NY, United States.
Max BrennerCenter for Immunology and Inflammation, Feinstein Institutes for Medical Research, Manhasset, NY, United States.
Ping WangCenter for Immunology and Inflammation, Feinstein Institutes for Medical Research, Manhasset, NY, United States.
Feinstein Institute for Medical Research · USDonald & Barbara Zucker School of Medicine at Hofstra/Northwell · USIcahn School of Medicine at Mount Sinai · US

Funding

IMPROVEMENT OF ORGAN FUNCTION AFTER SEVERE HYPOVOLEMIAR01HL076179 · NHLBI · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI PING WANG · 2004 to 2026
$7.6M
Novel Approaches to Maintaining Organ Function in SepsisR35GM118337 · NIGMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI PING WANG · 2016 to 2026
$5.2M
NHLBI NIH HHS R01 HL076179NIGMS NIH HHS R35 GM118337
6 · The paper itself

Abstract

Extracellular cold-inducible RNA-binding protein (eCIRP), a new damage-associated molecular pattern (DAMP), has been recently shown to play a critical role in promoting the development of bleomycin-induced pulmonary fibrosis. Although fibroblast activation is a critical component of the fibrotic process, the direct effects of eCIRP on fibroblasts have never been examined. We studied eCIRP's role in the induction of inflammatory phenotype in pulmonary fibroblasts and its connection to bleomycin-induced pulmonary fibrosis in mice. We found that eCIRP causes the induction of proinflammatory cytokines and differentially expression-related pathways in a TLR4-dependent manner in pulmonary fibroblasts. Our analysis further showed that the accessory pathways MD2 and Myd88 are involved in the induction of inflammatory phenotype. In order to study the connection of the enrichment of these pathways in priming the microenvironment for pulmonary fibrosis, we investigated the gene expression profile of lung tissues from mice subjected to bleomycin-induced pulmonary fibrosis collected at various time points. We found that at day 14, which corresponds to the inflammatory-to-fibrotic transition phase after bleomycin injection, TLR4, MD2, and Myd88 were induced, and the transcriptome was differentially enriched for genes in those pathways. Furthermore, we also found that inflammatory cytokines gene expressions were induced, and the cellular responses to these inflammatory cytokines were differentially enriched on day 14. Overall, our results show that eCIRP induces inflammatory phenotype in pulmonary fibroblasts in a TLR4 dependent manner. This study sheds light on the mechanism by which eCIRP induced inflammatory fibroblasts, contributing to pulmonary fibrosis.

Indexed as

AnimalsComputational BiologyCytokinesDisease Models, AnimalDisease SusceptibilityExtracellular SpaceFibroblastsGene ExpressionGene Expression ProfilingInflammationInflammation MediatorsMiceMice, KnockoutPhenotypePulmonary FibrosisRNA-Binding ProteinsCirbp protein, mouseCytokinesInflammation MediatorsRNA-Binding ProteinsToll-Like Receptor 4bleomicyneCIRPfibroblastfibrosisinflammation

Identifiers

PMID34367191
PMCPMC8342891
OpenAlexW3185822981

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.