Evidence map›Paper›PMID 17018860›Full record

ArticleBlood2007

Dual role for RhoA in suppression and induction of cytokines in the human neutrophil.

Michael B Fessler, Patrick G Arndt, Ingo Just, Jerry A Nick, Kenneth C Malcolm, G Scott Worthen

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Lysophosphatidylcholine induces azurophil granule translocationThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. 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

6 authors at 3 institutions in 2 countries.

Michael B FesslerDepartment of Medicine, National Jewish Medical and Research Center, Denver, CO, USA. fesslerm@niehs.nih.gov
Patrick G Arndt
Ingo Just
Jerry A Nick
Kenneth C Malcolm
G Scott Worthen
University of Colorado Denver · USNational Jewish Health · USMedizinische Hochschule Hannover · DE

Funding

Role of Interleukin-18 in Acute Lung InjuryP01HL068743 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ABRAHAM, EDWARD · 2002 to 2006
$7.4M
Cell Signaling of Host DefenseZ01ES102005 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI FESSLER, MICHAEL B · 2006 to 2008
$3.3M
LPS-INDUCED NEUTROPHIL ACCUMULATION IN THE LUNGR01HL061407 · NHLBI · NATIONAL JEWISH HEALTH · PI WORTHEN, GEORGE SCOTT · 1999 to 2007
$2.6M
Chemokine Compartmentalization and Neutrophil Accumulation in the LungR01HL105834 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI WORTHEN, GEORGE SCOTT · 2011 to 2014
$1.6M
The LPS Responsiveness of TLR2 an TLR4 in the NeutrophilK08HL067179 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ARNDT, PATRICK G · 2001 to 2005
$618k
NHLBI NIH HHS 5P01HL68743-04NHLBI NIH HHS 5R01HL061407-08NHLBI NIH HHS HL67179NHLBI NIH HHS K08 HL067179NHLBI NIH HHS P01 HL068743NHLBI NIH HHS R01 HL061407NHLBI NIH HHS R01 HL105834
6 · The paper itself

Abstract

Production of tumor necrosis factor-alpha (TNFalpha) by the neutrophil (PMN) is a pivotal event in innate immunity, but the signals regulating TNFalpha induction in this primary cell are poorly understood. Herein, we use protein transduction to identify novel, opposing anti- and pro-cytokine-inducing roles for RhoA in the resting and lipopolysaccharide (LPS)-stimulated human PMN, respectively. In the resting cell, RhoA suppresses Cdc42 activation, IkappaBalpha degradation, nuclear factor-kappaB (NF-kappaB) activation, and induction of TNFalpha and NF-kappaB-dependent chemokines. Suppression of TNFalpha induction by RhoA is Rho kinase alpha (ROCKalpha) independent, but Cdc42 dependent, because TNFalpha induction by C3 transferase is attenuated by inhibition of Cdc42, and constitutively active Cdc42 suffices to activate NF-kappaB and induce TNFalpha. By contrast, we also place RhoA downstream of p38 mitogen-activated protein kinase and Cdc42 in a novel LPS-activated pathway in which p38, Cdc42, and ROCKalpha all promote TNFalpha protein expression. The p65 subunit of NF-kappaB coprecipitates with RhoA in a manner sensitive to the RhoA activation state. Our findings suggest a new, 2-faced role for RhoA as a checkpoint in innate immunity.

Indexed as

Gene Expression Regulationcdc42 GTP-Binding ProteinCytokinesDown-RegulationHumansI-kappa B ProteinsImmunity, InnateNeutrophilsNF-kappa BNF-KappaB Inhibitor alpharhoA GTP-Binding ProteinTumor Necrosis Factor-alphaUp-Regulationcdc42 GTP-Binding ProteinCytokinesI-kappa B ProteinsNF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, humanrhoA GTP-Binding ProteinRHOA protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID17018860
PMCPMC1785129
OpenAlexW2010778539

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.