Evidence map›Paper›PMID 19079685›Full record

ArticleInternational journal of clinical and experimental medicine2008

beta-Arrestin 2: a Negative Regulator of Inflammatory Responses in Polymorphonuclear Leukocytes.

Fahmin Basher, Hongkuan Fan, Basilia Zingarelli, Keith T Borg, Lou M Luttrell, George E Tempel, Perry V Halushka, James A Cook

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. GABAPsychopharmacology · 2019
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Protective effects of dexamethasone on early acute lung injury induced by oleic acid in rats.International journal of clinical and experimental medicine · 2014
    Article
  13. Effect of penehyclidine hydrochloride on β-arrestin-1 expression in lipopolysaccharide-induced human pulmonary microvascular endothelial cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2013
    Article
  14. Article
  15. Article
  16. β-Arrestins in the immune system.Progress in molecular biology and translational science · 2013
    Review
  17. Article
  18. Article
  19. Review
  20. 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

8 authors.

Fahmin Basher
Hongkuan Fan
Basilia Zingarelli
Keith T Borg
Lou M Luttrell
George E Tempel
Perry V Halushka
James A Cook

Funding

The Role of Eicosanoids in ShockR01GM027673 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI COOK, JAMES A. · 1985 to 2015
$5.7M
PPARgamma and PPARgamma agonists in septic shockR01GM067202 · NIGMS · CINCINNATI CHILDRENS HOSP MED CTR · PI ZINGARELLI, BASILIA · 2003 to 2015
$3.9M
NIGMS NIH HHS R01 GM027673NIGMS NIH HHS R01 GM067202
6 · The paper itself

Abstract

Heterotrimeric Gi proteins have been previously implicated in signaling leading to inflammatory mediator production induced by bacterial lipopolysaccharide (LPS). beta-arrestins are ubiquitously expressed proteins that alter G-protein-coupled receptors signaling. beta-arrestin 2 plays a multifaceted role as a scaffold protein in regulating cellular inflammatory responses. Polymorphonuclear leukocytes (PMNs) activated by LPS induce inflammatory responses resulting in organ injury during sepsis. We hypothesized that beta-arrestin 2 is a critical modulator of inflammatory responses in PMNs. To examine the potential role of beta-arrestin 2 in LPS-induced cellular activation, we studied homozygous beta-arrestin 2 (-/-), heterozygous (+/-), and wildtype (+/+) mice. PMNs were stimulated with LPS for 16h. There was increased basal TNFalpha and IL-6 production in the beta-arrestin 2 (-/-) compared to both beta-arrestin 2 (+/-) and (+/+) cells. LPS failed to stimulate TNFalpha production in the beta-arrestin 2 (-/-) PMNs. However, LPS stimulated IL-6 production was increased in the beta-arrestin 2 (-/-) cells compared to (+/+) cells. In subsequent studies, peritoneal PMN recruitment was increased 81% in the beta-arrestin 2 (-/-) mice compared to (+/+) mice (p<0.05). beta-arrestin 2 deficiency resulted in an augmented expression of CD18 and CD62L (p<0.05). In subsequent studies, beta-arrestin 2 (-/-) and (+/+) mice were subjected to cecal ligation and puncture (CLP) and lung was collected and analyzed for myeloperoxidase activity (MPO) as index of PMNs infiltrate. CLP-induced MPO activity was significantly increased (p<0.05) in the beta-arrestin 2 (-/-) compared to (+/+) mice. These studies demonstrate that beta-arrestin 2 is a negative regulator of PMN activation and pulmomary leukosequestration in response to polymicrobial sepsis.

Indexed as

adhesion receptorslipopolysaccharide (LPS)Polymorphonuclear leukocytes (PMN)β-arrestin 2

Identifiers

PMID19079685
PMCPMC2596334
OpenAlexW97594156

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.