Evidence map›Paper›PMID 26799633›Full record

ArticlePloS one2016

AMPK-Activated Protein Kinase Suppresses Ccr2 Expression by Inhibiting the NF-κB Pathway in RAW264.7 Macrophages.

Fumiaki Kumase, Kimio Takeuchi, Yuki Morizane, Jun Suzuki, Hidetaka Matsumoto, Keiko Kataoka, Ahmad Al-Moujahed, Daniel E Maidana, Joan W Miller, Demetrios G Vavvas

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 33 citations in OpenAlex.

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  9. The energy sensor AMPK orchestrates metabolic and translational adaptation in expanding T helper cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  10. Antimicrobial agents and chemotherapy · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Fumiaki KumaseRetina Service, Angiogenesis Laboratory, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, United States of America.
Kimio TakeuchiRetina Service, Angiogenesis Laboratory, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, United States of America.
Yuki MorizaneRetina Service, Angiogenesis Laboratory, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, United States of America.
Jun SuzukiRetina Service, Angiogenesis Laboratory, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, United States of America.
Hidetaka MatsumotoRetina Service, Angiogenesis Laboratory, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, United States of America.
Keiko KataokaRetina Service, Angiogenesis Laboratory, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, United States of America.
Ahmad Al-MoujahedRetina Service, Angiogenesis Laboratory, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, United States of America.
Daniel E MaidanaRetina Service, Angiogenesis Laboratory, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, United States of America.
Joan W MillerRetina Service, Angiogenesis Laboratory, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, United States of America.
Demetrios G VavvasRetina Service, Angiogenesis Laboratory, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, United States of America.
Harvard University · USMassachusetts Eye and Ear Infirmary · US

Funding

P30 Core Grant for Vision ResearchP30EY014104 · NEI · MASSACHUSETTS EYE AND EAR INFIRMARY · PI Eric A Pierce · 2002 to 2026
$15.1M
Necroptosis, neuroprotection and axonal regeneration in retina ganglion cell injuryR01EY025362 · NEI · MASSACHUSETTS EYE AND EAR INFIRMARY · PI VAVVAS, DEMETRIOS · 2015 to 2018
$1.5M
Necroptosis and Neuroprotection in AMDR21EY023079 · NEI · MASSACHUSETTS EYE AND EAR INFIRMARY · PI VAVVAS, DEMETRIOS · 2013 to 2014
$404k
NEI NIH HHS EY014104NEI NIH HHS P30 EY014104NEI NIH HHS R01 EY025362NEI NIH HHS R21 EY023079NEI NIH HHS R21EY023079-01A1
6 · The paper itself

Abstract

C-C chemokine receptor 2 (Ccr2) is a key pro-inflammatory marker of classic (M1) macrophage activation. Although Ccr2 is known to be expressed both constitutively and inductively, the full regulatory mechanism of its expression remains unclear. AMP-activated protein kinase (AMPK) is not only a master regulator of energy homeostasis but also a central regulator of inflammation. In this study, we sought to assess AMPK's role in regulating RAW264.7 macrophage Ccr2 protein levels in resting (M0) or LPS-induced M1 states. In both M0 and M1 RAW264.7 macrophages, knockdown of the AMPKα1 subunit by siRNA led to increased Ccr2 levels whereas pharmacologic (A769662) activation of AMPK, attenuated LPS-induced increases in Ccr2 expression in an AMPK dependent fashion. The increases in Ccr2 levels by AMPK downregulation were partially reversed by NF-κB inhibition whereas TNF-a inhibition had minimal effects. Our results indicate that AMPK is a negative regulator of Ccr2 expression in RAW264.7 macrophages, and that the mechanism of action of AMPK inhibition of Ccr2 is mediated, in part, through the NF-κB pathway.

Indexed as

AMP-Activated Protein KinasesAnimalsCell LineEnzyme ActivationGene Expression RegulationInflammationLipopolysaccharidesMacrophage ActivationMacrophagesMiceNF-kappa BReceptors, CCR2RNA InterferenceRNA, Small InterferingSignal TransductionTumor Necrosis Factor-alphaAMP-Activated Protein KinasesCcr2 protein, mouseLipopolysaccharidesNF-kappa BPrkaa1 protein, mouseReceptors, CCR2RNA, Small InterferingTumor Necrosis Factor-alpha

Identifiers

PMID26799633
PMCPMC4723067
OpenAlexW2416103557

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.