Evidence map›Paper›PMID 29903736›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2018

Limited Macrophage Positional Dynamics in Progressing or Regressing Murine Atherosclerotic Plaques-Brief Report.

Jesse W Williams, Catherine Martel, Stephane Potteaux, Ekaterina Esaulova, Molly A Ingersoll, Andrew Elvington, Brian T Saunders, Li-Hao Huang, Andreas J Habenicht, Bernd H Zinselmeyer and 1 more

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In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

37 citing papers in PubMed, 53 citations in OpenAlex.

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  16. Article
  17. Survey of Approaches for Investigation of Atherosclerosis In Vivo.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  18. Macrophages in Atheromatous Plaque Developmental Stages.Frontiers in cardiovascular medicine · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Jesse W WilliamsFrom the Department of Pathology & Immunology, Washington University School of Medicine, St Louis, MO (J.W.W., C.M., E.E., A.E., B.T.S., L.-H.H., B.H.Z., G.J.R.).
Catherine MartelFrom the Department of Pathology & Immunology, Washington University School of Medicine, St Louis, MO (J.W.W., C.M., E.E., A.E., B.T.S., L.-H.H., B.H.Z., G.J.R.).
Stephane PotteauxDepartment of Gene and Cell Medicine, Mount Sinai School of Medicine, New York (S.P., M.A.I., G.J.R.).
Ekaterina EsaulovaFrom the Department of Pathology & Immunology, Washington University School of Medicine, St Louis, MO (J.W.W., C.M., E.E., A.E., B.T.S., L.-H.H., B.H.Z., G.J.R.).
Molly A IngersollDepartment of Gene and Cell Medicine, Mount Sinai School of Medicine, New York (S.P., M.A.I., G.J.R.).
Andrew ElvingtonFrom the Department of Pathology & Immunology, Washington University School of Medicine, St Louis, MO (J.W.W., C.M., E.E., A.E., B.T.S., L.-H.H., B.H.Z., G.J.R.).
Brian T SaundersFrom the Department of Pathology & Immunology, Washington University School of Medicine, St Louis, MO (J.W.W., C.M., E.E., A.E., B.T.S., L.-H.H., B.H.Z., G.J.R.).
Li-Hao HuangFrom the Department of Pathology & Immunology, Washington University School of Medicine, St Louis, MO (J.W.W., C.M., E.E., A.E., B.T.S., L.-H.H., B.H.Z., G.J.R.).
Andreas J HabenichtInstitute for Cardiovascular Prevention, Ludwig Maximilians University of Munich, Germany (A.J.H.).
Bernd H ZinselmeyerFrom the Department of Pathology & Immunology, Washington University School of Medicine, St Louis, MO (J.W.W., C.M., E.E., A.E., B.T.S., L.-H.H., B.H.Z., G.J.R.).
Gwendalyn J RandolphFrom the Department of Pathology & Immunology, Washington University School of Medicine, St Louis, MO (J.W.W., C.M., E.E., A.E., B.T.S., L.-H.H., B.H.Z., G.J.R.).
Washington University in St. Louis · USIcahn School of Medicine at Mount Sinai · US

Funding

DIABETES &RELATED METABOLIC DISEASEST32DK007120 · NIDDK · WASHINGTON UNIVERSITY · PI MARCO COLONNA, Maria Sara Remedi · 1986 to 2026
$15.7M
TRAINING PROGRAM IN IMMUNOLOGY AND IMMUNOGENETICST32AI007163 · NIAID · WASHINGTON UNIVERSITY · PI Kenneth M Murphy, Kodi S Ravichandran · 1985 to 2026
$14.8M
PRINCIPLES IN CARDIVASCULAR RESEARCH TRAINING PROGRAMT32HL007081 · NHLBI · WASHINGTON UNIVERSITY · PI Abhinav Diwan, Karen Ellen Joynt Maddox · 1985 to 2026
$10.6M
Differentiation/migratory fate of monocyte-derived cellsR01AI049653 · NIAID · WASHINGTON UNIVERSITY · PI Gwendalyn J Randolph · 2000 to 2026
$4.6M
DIFFERENTIATION AND FUNCTION OF MONOCYTES AND MACROPHAGESR37AI049653 · NIAID · WASHINGTON UNIVERSITY · PI RANDOLPH, GWENDALYN J · 2016 to 2025
$4.3M
INTEGRATING CELL & LIPOPROTEIN TRAFFICKING WITH VASCULAR BIOLOGY IN HUMAN IBDDP1DK109668 · NIDDK · WASHINGTON UNIVERSITY · PI RANDOLPH, GWENDALYN J · 2015 to 2019
$3.8M
VEGF-C/VEGFR3 AND LYMPHATIC TRANSPORT OF CHOLESTEROL FROM ATHEROSCLEROTIC PLAQUER01HL118206 · NHLBI · WASHINGTON UNIVERSITY · PI RANDOLPH, GWENDALYN J · 2014 to 2017
$1.5M
ATHEROSCLEROTIC LESION INITIATION BY RESIDENT AORTIC MACROPHAGE PROLIFERATION AND LIPID UPTAKEK99HL138163 · NHLBI · WASHINGTON UNIVERSITY · PI WILLIAMS, JESSE WARREN · 2018 to 2018
$125k
NHLBI NIH HHS K99 HL138163NHLBI NIH HHS R01 HL118206NHLBI NIH HHS T32 HL007081NIAID NIH HHS R01 AI049653NIAID NIH HHS R37 AI049653NIAID NIH HHS T32 AI007163NIDDK NIH HHS DP1 DK109668NIDDK NIH HHS T32 DK007120
6 · The paper itself

Abstract

Objective- Macrophages play important roles in the pathogenesis of atherosclerosis, but their dynamics within plaques remain obscure. We aimed to quantify macrophage positional dynamics within progressing and regressing atherosclerotic plaques. Approach and Results- In a stable intravital preparation, large asymmetrical foamy macrophages in the intima of carotid artery plaques were sessile, but smaller rounded cells nearer plaque margins, possibly newly recruited monocytes, mobilized laterally along plaque borders. Thus, to test macrophage dynamics in plaques over a longer period of time in progressing and regressing disease, we quantified displacement of nondegradable phagocytic particles within macrophages for up to 6 weeks. In progressing plaques, macrophage-associated particles appeared to mobilize to deeper layers in plaque, whereas in regressing plaques, the label was persistently located near the lumen. By measuring the distance of the particles from the floor of the plaque, we discovered that particles remained at the same distance from the floor regardless of plaque progression or regression. The apparent deeper penetration of labeled cells in progressing conditions could be attributed to monocyte recruitment that generated new superficial layers of macrophages over the labeled phagocytes. Conclusions- Although there may be individual exceptions, as a population, newly differentiated macrophages fail to penetrate significantly deeper than the limited depth they reside on initial entry, regardless of plaque progression, or regression. These limited dynamics may prevent macrophages from escaping areas with unfavorable conditions (such as hypoxia) and pose a challenge for newly recruited macrophages to clear debris through efferocytosis deep within plaque.

Indexed as

Plaque, AtheroscleroticAnimalsAortaAortic DiseasesAtherosclerosisCarotid ArteriesCarotid Artery DiseasesCell DifferentiationCell MovementDisease Models, AnimalDisease ProgressionFemaleMacrophagesMaleMice, Inbred C57BLMice, Knockout, ApoECcr2 protein, mouseReceptors, CCR2Receptors, LDLarteriosclerosiscell adhesioninflammationintravital microscopymonocytes

Identifiers

PMID29903736
PMCPMC6202234
OpenAlexW2886387637

What OpenQuestion holds

Textmetadata
LicenceTDM
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.