Evidence map›Paper›PMID 27349568›Full record

ArticleScientific reports2016

WISP1-αvβ3 integrin signaling positively regulates TLR-triggered inflammation response in sepsis induced lung injury.

Zhixia Chen, Xibing Ding, Shuqing Jin, Bruce Pitt, Liming Zhang, Timothy Billiar, Quan Li

Abstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. An overview of CCN4 (WISP1) role in human diseases.Journal of translational medicine · 2024
    Review
  5. Review
  6. Toll-like receptors and integrins crosstalk.Frontiers in immunology · 2024
    Review
  7. Optimal CCN4 Immunofluorescence for Tissue Microarray.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
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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

7 authors.

Zhixia ChenDepartment of Anesthesiology, East Hospital, Tongji University school of Medicine, Shanghai, China.
Xibing DingDepartment of Anesthesiology, East Hospital, Tongji University school of Medicine, Shanghai, China.
Shuqing JinDepartment of Anesthesiology, East Hospital, Tongji University school of Medicine, Shanghai, China.
Bruce PittDepartment of Environmental and Occupational Health, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
Liming ZhangDepartment of Anesthesiology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, United States of America.
Timothy BilliarDepartment of Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, United States of America.
Quan LiDepartment of Anesthesiology, East Hospital, Tongji University school of Medicine, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We recently noted that the matricellular protein WISP1 contributes to sepsis induced acute lung injury (ALI) via integrin β6. In the current study, we pursued further aspects of WISP1 modulation of TLR signaling in lungs of mice after sepsis and TLR4 mediated release of TNF-α in macrophages. After confirming that TLR4 and CD14 are critical in transducing sepsis mediated ALI, we now demonstrate that intrapulmonary αvβ3 is increased by polymicrobrial sepsis in a TLR4, CD14 dependent fashion. Comparison of cultured macrophages revealed that WISP1 increased release of TNF-α from RAW264.7 cells with baseline expression of αvβ3, but primary cultures of peritoneal macrophages (PMø) required activation of TLR4 to induce de novo synthesis of αvβ3 enabling WISP1 to stimulate release of TNF-α. The specific requirement for β3 integrin was apparent when the effect of WISP1 was lost in PMø isolated from β3(-/-) mice. WISP1 enhanced TLR4 mediated ERK signaling and U0126 (an ERK inhibitor) blocked LPS induced β3 integrin expression and WISP1 enhanced TNF-α release. Collectively these data suggest that WISP1-αvβ3 integrin signaling is involved in TLR4 pathways in macrophages and may be an important contributor to TLR4/CD14 mediated inflammation in sepsis induced lung injury.

Indexed as

Acute Lung InjuryAnimalsCCN Intercellular Signaling ProteinsCells, CulturedInflammationIntegrin alphaVbeta3MacrophagesMacrophages, PeritonealMiceMice, Inbred C57BLMice, KnockoutProto-Oncogene ProteinsRAW 264.7 CellsRecombinant ProteinsSepsisSignal TransductionCCN4 protein, mouseCCN Intercellular Signaling ProteinsIntegrin alphaVbeta3Proto-Oncogene ProteinsRecombinant ProteinsToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID27349568
PMCPMC4923866

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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.