Evidence map›Paper›PMID 35681501›Full record

ArticleCells2022

The Actin Cytoskeleton Responds to Inflammatory Cues and Alters Macrophage Activation.

Elsa Ronzier, Alexander J Laurenson, Rohini Manickam, Sophia Liu, Imelda M Saintilma, Dillon C Schrock, John A Hammer, Jeremy D Rotty

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.5field-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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Isolation of Human Osteal Macrophages.Life (Basel, Switzerland) · 2026
    Article
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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

8 authors at 4 institutions in 1 country.

Elsa RonzierDepartment of Biochemistry and Molecular Biology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
Alexander J LaurensonDepartment of Biochemistry and Molecular Biology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
Rohini ManickamDepartment of Biochemistry and Molecular Biology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
Sophia LiuDepartment of Biochemistry and Molecular Biology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
Imelda M SaintilmaDepartment of Biochemistry and Molecular Biology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
Dillon C SchrockCell and Developmental Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.
John A HammerCell and Developmental Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Jeremy D RottyDepartment of Biochemistry and Molecular Biology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
Henry M. Jackson Foundation · USUniformed Services University of the Health Sciences · USNational Heart Lung and Blood Institute · USNational Institutes of Health · US

Funding

Roles of cytoskektal dynamics in T lymphocyte functionZIAHL006121 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI HAMMER, JOHN A · 2011 to 2025
$19.8M
Extracellular matrix sensing in cellular signaling, migration and wound repairR01GM134104 · NIGMS · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI ROTTY, JEREMY · 2019 to 2023
$1.6M
Intramural NIH HHS ZIA HL006121NIGMS NIH HHS R01 GM134104
6 · The paper itself

Abstract

Much remains to be learned about the molecular mechanisms underlying a class of human disorders called actinopathies. These genetic disorders are characterized by loss-of-function mutations in actin-associated proteins that affect immune cells, leading to human immunopathology. However, much remains to be learned about how cytoskeletal dysregulation promotes immunological dysfunction. The current study reveals that the macrophage actin cytoskeleton responds to LPS/IFNγ stimulation in a biphasic manner that involves cellular contraction followed by cellular spreading. Myosin II inhibition by blebbistatin blocks the initial contraction phase and lowers iNOS protein levels and nitric oxide secretion. Conversely, conditional deletion of Arp2/3 complex in macrophages attenuates spreading and increases nitric oxide secretion. However, iNOS transcription is not altered by loss of myosin II or Arp2/3 function, suggesting post-transcriptional regulation of iNOS by the cytoskeleton. Consistent with this idea, proteasome inhibition reverses the effects of blebbistatin and rescues iNOS protein levels. Arp2/3-deficient macrophages demonstrate two additional phenotypes: defective MHCII surface localization, and depressed secretion of the T cell chemokine CCL22. These data suggest that interplay between myosin II and Arp2/3 influences macrophage activity, and potentially impacts adaptive-innate immune coordination. Disrupting this balance could have detrimental impacts, particularly in the context of Arp2/3-associated actinopathies.

Indexed as

Macrophage ActivationNitric OxideActin CytoskeletonActin-Related Protein 2-3 ComplexActinsCuesMyosin Type IIActin-Related Protein 2-3 ComplexActinsMyosin Type IINitric Oxideactin cytoskeletonArp2/3 complexCCL22inflammationiNOSmacrophagesmyosin-II

Identifiers

PMID35681501
PMCPMC9180445
OpenAlexW4281703590

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.