Evidence map›Paper›PMID 22647600›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Akt1 and Akt2 protein kinases differentially contribute to macrophage polarization.

Alicia Arranz, Christina Doxaki, Eleni Vergadi, Yeny Martinez de la Torre, Katerina Vaporidi, Eleni D Lagoudaki, Eleftheria Ieronymaki, Ariadne Androulidaki, Maria Venihaki, Andrew N Margioris and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 339 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
339citing papers in PubMed, 4 pooled it
13.4field-weighted citation impact, top 1% 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

339 citing papers in PubMed, 4 syntheses or guidelines pooled it, 599 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Targeting USP47 reprograms macrophage polarization to ameliorate septic peritonitis and promote cutaneous wound healing.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  17. A genome-wide CRISPR screen defines host determinants of earlybioRxiv : the preprint server for biology · 2026
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279 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

13 authors at 3 institutions in 2 countries.

Alicia ArranzDepartment of Clinical Chemistry, School of Medicine, University of Crete, Heraklion 71003, Crete, Greece.
Christina Doxaki
Eleni Vergadi
Yeny Martinez de la Torre
Katerina Vaporidi
Eleni D Lagoudaki
Eleftheria Ieronymaki
Ariadne Androulidaki
Maria Venihaki
Andrew N Margioris
Efstathios N Stathopoulos
Philip N Tsichlis
Christos Tsatsanis
University of Crete · GRMolecular Oncology (United States) · USTufts Medical Center · US

Funding

Akt in T cell development and functionR01CA057436 · NCI · TUFTS MEDICAL CENTER · PI TSICHLIS, PHILIP N. · 1994 to 2011
$3.2M
NCI NIH HHS R01 CA057436NCI NIH HHS R01-CA057436Worldwide Cancer Research 11-0505
6 · The paper itself

Abstract

Activated macrophages are described as classically activated or M1 type and alternatively activated or M2 type, depending on their response to proinflammatory stimuli and the expression of genetic markers including iNOS, arginase1, Ym1, and Fizz1. Here we report that Akt kinases differentially contribute to macrophage polarization, with Akt1 ablation giving rise to an M1 and Akt2 ablation resulting in an M2 phenotype. Accordingly, Akt2(-/-) mice were more resistant to LPS-induced endotoxin shock and to dextran sulfate sodium (DSS)-induced colitis than wild-type mice, whereas Akt1(-/-) mice were more sensitive. Cell depletion and reconstitution experiments in a DSS-induced colitis model confirmed that the effect was macrophage-dependent. Gene-silencing studies showed that the M2 phenotype of Akt2(-/-) macrophages was cell autonomous. The microRNA miR-155, whose expression was repressed in naive and in LPS-stimulated Akt2(-/-) macrophages, and its target C/EBPβ appear to play a key role in this process. C/EBPβ, a hallmark of M2 macrophages that regulates Arg1, was up-regulated upon Akt2 ablation or silencing. Overexpression or silencing of miR-155 confirmed its central role in Akt isoform-dependent M1/M2 polarization of macrophages.

Indexed as

Cell PolarityAnimalsMacrophagesMiceProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-akt

Identifiers

PMID22647600
PMCPMC3386059
OpenAlexW1981056356

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.