Evidence map›Paper›PMID 24081661›Full record

ArticleBlood2013

Elevated CXCL1 expression in gp130-deficient endothelial cells impairs neutrophil migration in mice.

Longbiao Yao, Tadayuki Yago, Bojing Shao, Zhenghui Liu, Robert Silasi-Mansat, Hendra Setiadi, Florea Lupu, Rodger P McEver

Abstract read
In one paragraph

Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Longbiao YaoCardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK; and.
Tadayuki Yago
Bojing Shao
Zhenghui Liu
Robert Silasi-Mansat
Hendra Setiadi
Florea Lupu
Rodger P McEver
Oklahoma Medical Research Foundation · US

Funding

Protein-glycan Interactions in the Vascular SystemP01HL085607 · NHLBI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI CUMMINGS, RICHARD D, MCEVER, RODGER PAUL · 2006 to 2015
$16.8M
SWI/SNF-REGULATED POSTNATAL ANGIOGENESISP20RR018758 · NCRR · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI XIA, LIJUN · 2003 to 2011
$14.9M
Interdisciplinary research in vascular biologyP20GM103441 · NIGMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI MCEVER, RODGER PAUL · 2012 to 2014
$7.3M
Signal-dependent neutrophil adhesion to vascular surfacesR01HL034363 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI MCEVER, RODGER PAUL · 1985 to 2017
$3.9M
CYTOPLASMIC REGULATION OF P-SELECTIN/PSGL-1 INTERACTIONSR37HL034363 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI MCEVER, RODGER PAUL · 1998 to 2007
$3.3M
NCRR NIH HHS P20 RR018758NHLBI NIH HHS HL034363NHLBI NIH HHS HL085607NHLBI NIH HHS P01 HL085607NHLBI NIH HHS R01 HL034363NHLBI NIH HHS R37 HL034363NIGMS NIH HHS GM103441NIGMS NIH HHS P20 GM103441
6 · The paper itself

Abstract

Neutrophils emigrate from venules to sites of infection or injury in response to chemotactic gradients. How these gradients form is not well understood. Some IL-6 family cytokines stimulate endothelial cells to express adhesion molecules and chemokines that recruit leukocytes. Receptors for these cytokines share the signaling subunit gp130. We studied knockout mice lacking gp130 in endothelial cells. Unexpectedly, gp130-deficient endothelial cells constitutively expressed more CXCL1 in vivo and in vitro, and even more upon stimulation with tumor necrosis factor-α. Mobilization of this increased CXCL1 from intracellular stores to the venular surface triggered β2 integrin-dependent arrest of neutrophils rolling on selectins but impaired intraluminal crawling and transendothelial migration. Superfusing CXCL1 over venules promoted neutrophil migration only after intravenously injecting mAb to CXCL1 to diminish its intravascular function or heparinase to release CXCL1 from endothelial proteoglycans. Remarkably, mice lacking gp130 in endothelial cells had impaired histamine-induced venular permeability, which was restored by injecting anti-P-selectin mAb to prevent neutrophil rolling and arrest. Thus, excessive CXCL1 expression in gp130-deficient endothelial cells augments neutrophil adhesion but hinders migration, most likely by disrupting chemotactic gradients. Our data define a role for endothelial cell gp130 in regulating integrin-dependent adhesion and de-adhesion of neutrophils during inflammation.

Indexed as

AnimalsCapillary PermeabilityCell AdhesionCell MovementChemokine CXCL1Cytokine Receptor gp130Endothelial CellsInflammationLeukocyte RollingMiceMice, Inbred C57BLMice, KnockoutNeutrophilsP-SelectinRNA, MessengerTumor Necrosis Factor-alphaChemokine CXCL1Cxcl1 protein, mouseCytokine Receptor gp130Il6st protein, mouseP-SelectinRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID24081661
PMCPMC3843240
OpenAlexW2045729584

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.