Evidence map›Paper›PMID 19622728›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Akt1 is critical for acute inflammation and histamine-mediated vascular leakage.

Annarita Di Lorenzo, Carlos Fernández-Hernando, Giuseppe Cirino, William C Sessa

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

105 citing papers in PubMed, 182 citations in OpenAlex.

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45 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

Annarita Di LorenzoDepartment of Pharmacology and Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT 06520, USA.
Carlos Fernández-Hernando
Giuseppe Cirino
William C Sessa
Yale University · USUniversity of Naples Federico II · IT

Funding

SOCS-1 and endothelial dysfunction in graft arteriosclerosisP01HL070295 · NHLBI · YALE UNIVERSITY · PI BENDER, JEFFREY R. · 2001 to 2010
$17.9M
PHOSPHORYLATION AND ENDOTHELIAL NITRIC OXIDE PRODUCTIONR01HL064793 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2000 to 2016
$6.3M
Endothelial NOS by Protein-Protein IntractionsR01HL061371 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 1999 to 2008
$3.6M
microRNA regulation of endothelial functionsR01HL096670 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2010 to 2013
$1.8M
Vascular Remodeling: Role of Nitric OxideR01HL057665 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C. · 1996 to 2004
$1.5M
NHLBI PROTEOMICS INITIATIVE-N01HV28186N01HV028186 · HV · YALE UNIVERSITY · PI WILLIAMS, KENNETH · 2002 to 2006
–
NHLBI NIH HHS N01 HV028186NHLBI NIH HHS N01-HV-28186NHLBI NIH HHS P01 HL070295NHLBI NIH HHS P01 HL70295NHLBI NIH HHS R01 HL057665NHLBI NIH HHS R01 HL061371NHLBI NIH HHS R01 HL064793NHLBI NIH HHS R01 HL096670NHLBI NIH HHS R01 HL57665NHLBI NIH HHS R01 HL61371NHLBI NIH HHS R01 HL64793
6 · The paper itself

Abstract

Akt1 is implicated in cell metabolism, survival migration, and gene expression; however, little is known about the role of specific Akt isoforms during inflammation in vivo. Thus, we directly explored the roles of the isoforms Akt1 and Akt2 in acute inflammation models by using mice deficient in either Akt1 or Akt2. Akt1(-/-) mice showed a markedly reduced edema versus Akt2(-/-) and WT controls, and the reduced inflammation was associated with a dramatic decrease in neutrophil and monocyte infiltration. The loss of Akt1 did not affect leukocyte functions in vitro, and bone marrow transplant experiments suggest that host Akt1 regulates leukocyte emigration into inflamed tissues. Moreover, carrageenan-induced edema and the direct propermeability actions of bradykinin and histamine were reduced dramatically in Akt1(-/-) versus WT mice. These findings are supported by in vitro experiments showing that Akt1 deficiency or blockade of nitric oxide synthase markedly reduces histamine-stimulated changes in transendothelial electrical resistance of microvascular endothelial cells. Collectively, these results suggest that Akt1 is necessary for acute inflammation and exerts its actions primarily via regulation of vascular permeability, leading to edema and leukocyte extravasation.

Indexed as

Acute DiseaseAnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticBlotting, WesternBone Marrow CellsBone Marrow TransplantationCapillary PermeabilityCarrageenanCD68 MoleculeCell MovementEdemaGene ExpressionHistamineImmunohistochemistryInflammationAkt1 protein, mouseAkt2 protein, mouseAntigens, CDAntigens, Differentiation, MyelomonocyticCarrageenanCD68 antigen, humanCD68 MoleculeHistaminePeroxidaseProto-Oncogene Proteins c-akt

Identifiers

PMID19622728
PMCPMC2732859
OpenAlexW2113752602

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.