Evidence map›Paper›PMID 31365293›Full record

ArticleAmerican journal of physiology. Cell physiology2019

Downregulation of calponin 2 contributes to the quiescence of lung macrophages.

Olesya Plazyo, Juan-Juan Sheng, J-P Jin

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.3field-weighted citation impact, top 40% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Evolution and function of calponin and transgelin.Frontiers in cell and developmental biology · 2023
    Review
  8. Article
  9. A rapid degradation of calponin 2 is required for cytokinesis.American journal of physiology. Cell physiology · 2021
    Article
  10. Article
  11. 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

3 authors at 1 institution in 1 country.

Olesya PlazyoDepartment of Physiology, Wayne State University School of Medicine, Detroit, Michigan.
Juan-Juan ShengDepartment of Physiology, Wayne State University School of Medicine, Detroit, Michigan.
J-P JinDepartment of Physiology, Wayne State University School of Medicine, Detroit, Michigan.
Wayne State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calponin 2 is an actin cytoskeleton-associated regulatory protein that inhibits the activity of myosin-ATPase and cytoskeleton dynamics. Recent studies have demonstrated that deletion of calponin 2 restricts the proinflammatory activation of macrophages in atherosclerosis and arthritis to attenuate the disease progression in mice. Here we demonstrate that the levels of calponin 2 vary among different macrophage populations, which may reflect their adaptation to specific tissue microenvironment corresponding to specific functional states. Interestingly, lung resident macrophages express significantly lower calponin 2 than peritoneal resident macrophages, which correlates with decreased substrate adhesion and reduced expression of proinflammatory cytokines and a proresolution phenotype. Deletion of calponin 2 in peritoneal macrophages also decreased substrate adhesion and downregulated the expression of proinflammatory cytokines. Providing the first line of defense against microbial invasion while receiving constant exposure to extrinsic antigens, lung macrophages need to maintain a necessary level of activity while limiting exaggerated inflammatory reaction. Therefore, their low level of calponin 2 may reflect an important physiological adaption. Downregulation of calponin 2 in macrophages may be targeted as a cytoskeleton-based novel mechanism, possibly via endoplasmic reticulum stress altering the processing and secretion of cytokines, to regulate immune response and promote quiescence for the treatment of inflammatory diseases.

Indexed as

ActinsAnimalsCalcium-Binding ProteinsCalponinsCell MovementCytokinesCytoskeletonDown-RegulationLungMacrophagesMacrophages, AlveolarMice, Inbred C57BLMice, TransgenicMicrofilament ProteinsMyosinsActinsCalcium-Binding ProteinsCalponinsCytokinesMicrofilament ProteinsMyosinsactinadhesioncytoskeletoninflammationmacrophage

Identifiers

PMID31365293
PMCPMC6850996
OpenAlexW2966768088

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.