Evidence map›Paper›PMID 29794410›Full record

ArticleJournal of atherosclerosis and thrombosis2018

Relationship between CCL22 Expression by Vascular Smooth Muscle Cells and Macrophage Histamine Receptors in Atherosclerosis.

Satoshi Kimura, Hirotsugu Noguchi, Uki Nanbu, Ke-Yong Wang, Yasuyuki Sasaguri, Toshiyuki Nakayama

Open access · diamondAbstract read
In one paragraph

Article in Journal of atherosclerosis and thrombosis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

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  4. Blocking HJournal of molecular medicine (Berlin, Germany) · 2024
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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

6 authors at 1 institution in 1 country.

Satoshi KimuraDepartment of Pathology, School of Medicine, University of Occupational and Environmental Health.
Hirotsugu NoguchiDepartment of Pathology, School of Medicine, University of Occupational and Environmental Health.
Uki NanbuDepartment of Pathology, School of Medicine, University of Occupational and Environmental Health.
Ke-Yong WangShared-Use Research Center, University of Occupational and Environmental Health.
Yasuyuki SasaguriDepartment of Pathology, School of Medicine, University of Occupational and Environmental Health.
Toshiyuki NakayamaDepartment of Pathology, School of Medicine, University of Occupational and Environmental Health.
University of Occupational and Environmental Health Japan · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimCCL22, mainly synthesized by monocyte-derived alternative (M2) macrophages, belongs to the CC family of chemokines and is involved in monocyte migration and recruitment. We have previously investigated CCL22 and histamine in atherosclerosis. Here, we investigated the hypothesis that CCL22 is involved in atherosclerosis, which is influenced by the differentiation of macrophage phenotypes via histamine.

methodsCCL22 expression was investigated in human carotid arteries and coronary arteries with bare metal stents. Ligated carotid arteries of wild-type (C57BL/6J) and apolipoprotein E-deficient mice were also used as atherosclerotic models. The localization and expression of CCL22 and classical (M1)-like and M2-like macrophages in various human and mouse atherosclerotic lesions were investigated by immunohistochemical examination and quantitative real-time polymerase chain reaction. Histamine is expressed in atherosclerosis, and it induces inflammation and immunity. Human- and mice-derived monocytes and macrophages were used to examine the role of histamine in macrophage differentiation and CCL22-expression. Macrophages derived from histamine receptor 1 (H1R)- and 2 (H2R)-knockout (KO) mice were also examined.

resultsAtherosclerotic lesions showed a distribution of heterogeneous macrophage phenotypes with M1-like and M2-like macrophage dominant sites. CCL22 was distributed in sparse areas of vascular smooth muscle cells (VSMCs) and associated with M2-like macrophages. Moreover, H2R stimulation was associated with CCL22 expression via M2-like macrophage dominant differentiation.

conclusionThe expression of M1- or M2-like macrophages in atherosclerosis were observed to be dependent on the distribution of VSMCs owing to differences in causal stimuli and the switching of histamine receptors via Th1 or Th2 cytokines. These results suggest that CCL22 may control atherosclerosis.

Indexed as

AnimalsApolipoproteins EAtherosclerosisBiomarkersCells, CulturedChemokine CCL22HumansMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutMuscle, Smooth, VascularReceptors, Histamine H1Receptors, Histamine H2Apolipoproteins EBiomarkersChemokine CCL22Receptors, Histamine H1Receptors, Histamine H2AtherosclerosisCCL22ChemokineHistamineMacrophage

Identifiers

PMID29794410
PMCPMC6249366
OpenAlexW2804291583

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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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.