Evidence map›Paper›PMID 27488671›Full record

ArticleAmerican journal of physiology. Cell physiology2016

Deletion of calponin 2 in macrophages attenuates the severity of inflammatory arthritis in mice.

Qi-Quan Huang, M Moazzem Hossain, Wen Sun, Lianping Xing, Richard M Pope, J-P Jin

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 16% 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, 24 citations in OpenAlex.

  1. Genetic evidence and cross-species functional characterization implicateProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Evolution and function of calponin and transgelin.Frontiers in cell and developmental biology · 2023
    Review
  11. Article
  12. Article
  13. Downregulation of calponin 2 contributes to the quiescence of lung macrophages.American journal of physiology. Cell physiology · 2019
    Article
  14. Article
  15. Article
  16. Article
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

6 authors at 3 institutions in 1 country.

Qi-Quan HuangDivision of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, Illinois; and.
M Moazzem HossainDepartment of Physiology, Wayne State University School of Medicine, Detroit, Michigan.
Wen SunDepartment of Pathology, University of Rochester, Rochester, New York.
Lianping XingDepartment of Pathology, University of Rochester, Rochester, New York.
Richard M PopeDivision of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, Illinois; and.
J-P JinDepartment of Physiology, Wayne State University School of Medicine, Detroit, Michigan; jjin@med.wayne.edu.
Northwestern University · USUniversity of Rochester · USWayne State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calponin is an actin cytoskeleton-associated protein that regulates motility-based cellular functions. Three isoforms of calponin are present in vertebrates, among which calponin 2 encoded by the Cnn2 gene is expressed in multiple types of cells, including blood cells from the myeloid lineage. Our previous studies demonstrated that macrophages from Cnn2 knockout (KO) mice exhibit increased migration and phagocytosis. Intrigued by an observation that monocytes and macrophages from patients with rheumatoid arthritis had increased calponin 2, we investigated anti-glucose-6-phosphate isomerase serum-induced arthritis in Cnn2-KO mice for the effect of calponin 2 deletion on the pathogenesis and pathology of inflammatory arthritis. The results showed that the development of arthritis was attenuated in systemic Cnn2-KO mice with significantly reduced inflammation and bone erosion than that in age- and stain background-matched C57BL/6 wild-type mice. In vitro differentiation of calponin 2-null mouse bone marrow cells produced fewer osteoclasts with decreased bone resorption. The attenuation of inflammatory arthritis was confirmed in conditional myeloid cell-specific Cnn2-KO mice. The increased phagocytotic activity of calponin 2-null macrophages may facilitate the clearance of autoimmune complexes and the resolution of inflammation, whereas the decreased substrate adhesion may reduce osteoclastogenesis and bone resorption. The data suggest that calponin 2 regulation of cytoskeleton function plays a novel role in the pathogenesis of inflammatory arthritis, implicating a potentially therapeutic target.

Indexed as

AnimalsArthritisBone ResorptionCalcium-Binding ProteinsCalponinsCell DifferentiationCytoskeletonGene DeletionGlucose-6-Phosphate IsomeraseHumansInflammationMacrophagesMiceMice, Inbred C57BLMice, KnockoutMicrofilament ProteinsCalcium-Binding ProteinsCalponinsGlucose-6-Phosphate IsomeraseMicrofilament Proteinscalponin 2cell adhesioninflammatory arthritismacrophagesosteoclasts

Identifiers

PMID27488671
PMCPMC5129749
OpenAlexW2506296588

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.