Evidence map›Paper›PMID 24196963›Full record

ArticleThe Journal of biological chemistry2013

Ezrin-radixin-moesin-binding phosphoprotein 50 (EBP50) and nuclear factor-κB (NF-κB): a feed-forward loop for systemic and vascular inflammation.

Kristen L Leslie, Gyun Jee Song, Stacey Barrick, Vanessa L Wehbi, Jean-Pierre Vilardaga, Philip M Bauer, Alessandro Bisello

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. 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
0.7field-weighted citation impact, top 28% 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, 30 citations in OpenAlex.

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  7. A Critical Role for NaJournal of immunology (Baltimore, Md. : 1950) · 2021
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  12. New roles of the NaAmerican journal of physiology. Renal physiology · 2020
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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 at 1 institution in 1 country.

Kristen L LeslieFrom the Department of Pharmacology and Chemical Biology.
Gyun Jee Song
Stacey Barrick
Vanessa L Wehbi
Jean-Pierre Vilardaga
Philip M Bauer
Alessandro Bisello
University of Pittsburgh · US

Funding

UNIVERSITY OF PITTSBURGH CLINICAL AND TRANSLATIONAL SCIENCE INSTITUTE: BPCAUL1RR024153 · NCRR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2006 to 2011
$73.9M
University of Pittsburgh Clinical and Translational Science InstituteUL1TR000005 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2012 to 2015
$50.8M
PREDOCTORAL TRAINING IN PHARMACOLOGICAL SCIENCEST32GM008424 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI PAGANO, PATRICK J · 1994 to 2019
$3.4M
Role of TRP channels in secondary injury after brain traumaR01NS072501 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI GERZANICH, VLADIMIR · 2011 to 2014
$1.3M
NCATS NIH HHS UL1 TR000005NCATS NIH HHS UL1TR000005NCRR NIH HHS UL1 RR024153NIGMS NIH HHS T32 GM008424NINDS NIH HHS NS072501
6 · The paper itself

Abstract

The interaction between vascular cells and macrophages is critical during vascular remodeling. Here we report that the scaffolding protein, ezrin-binding phosphoprotein 50 (EBP50), is a central regulator of macrophage and vascular smooth muscle cells (VSMC) function. EBP50 is up-regulated in intimal VSMC following endoluminal injury and promotes neointima formation. However, the mechanisms underlying these effects are not fully understood. Because of the fundamental role that inflammation plays in vascular diseases, we hypothesized that EBP50 mediates macrophage activation and the response of vessels to inflammation. Indeed, EBP50 expression increased in primary macrophages and VSMC, and in the aorta of mice, upon treatment with LPS or TNFα. This increase was nuclear factor-κB (NF-κB)-dependent. Conversely, activation of NF-κB was impaired in EBP50-null VSMC and macrophages. We found that inflammatory stimuli promote the formation of an EBP50-PKCζ complex at the cell membrane that induces NF-κB signaling. Macrophage activation and vascular inflammation after acute LPS treatment were reduced in EBP50-null cells and mice as compared with WT. Furthermore, macrophage recruitment to vascular lesions was significantly reduced in EBP50 knock-out mice. Thus, EBP50 and NF-κB participate in a feed-forward loop leading to increased macrophage activation and enhanced response of vascular cells to inflammation.

Indexed as

Feedback, PhysiologicalAnimalsAortaHumansHuman Umbilical Vein Endothelial CellsLipopolysaccharidesMacrophagesMiceMice, Inbred C57BLMyocytes, Smooth MuscleNF-kappa BPhosphoproteinsProtein Kinase CProtein Kinase C zetaSodium-Hydrogen ExchangersTumor Necrosis Factor-alphaLipopolysaccharidesNF-kappa BPhosphoproteinsProtein Kinase CProtein Kinase C zetasodium-hydrogen exchanger regulatory factorSodium-Hydrogen ExchangersTumor Necrosis Factor-alphaEBP50InflammationMacrophagesNF-Kappa B (NF-KB)NHERF1PDZ DomainPKC ZetaScaffold ProteinsVascular BiologyVascular Smooth Muscle Cells

Identifiers

PMID24196963
PMCPMC3868756
OpenAlexW2064834068

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.