Cited by 262Phagocytosis and Immune RegulationAtherosclerosis and Cardiovascular DiseasesCholesterol and Lipid Metabolism

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MerTK receptor cleavage promotes plaque necrosis and defective resolution in atherosclerosis

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Cai, Bishuang, Thorp, Edward B., Doran, Amanda C., Sansbury, Brian E., Daemen, Mat J.A.P., Dorweiler, Bernhard, Spite, Matthew, Fredman, Gabrielle, Tabas, Ira·2017·Journal of Clinical Investigation

DOI 10.1172/jci90520PMC PMC5272169

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Abstract

Atherothrombotic vascular disease is often triggered by a distinct type of atherosclerotic lesion that displays features of impaired inflammation resolution, notably a necrotic core and thinning of a protective fibrous cap that overlies the core. A key cause of plaque necrosis is defective clearance of apoptotic cells, or efferocytosis, by lesional macrophages, but the mechanisms underlying defective efferocytosis and its possible links to impaired resolution in atherosclerosis are incompletely understood. Here, we provide evidence that proteolytic cleavage of the macrophage efferocytosis receptor c-Mer tyrosine kinase (MerTK) reduces efferocytosis and promotes plaque necrosis and defective resolution. In human carotid plaques, MerTK cleavage correlated with plaque necrosis and the presence of ischemic symptoms. Moreover, in fat-fed LDL receptor-deficient (Ldlr-/-) mice whose myeloid cells expressed a cleavage-resistant variant of MerTK, atherosclerotic lesions exhibited higher macrophage MerTK, lower levels of the cleavage product soluble Mer, improved efferocytosis, smaller necrotic cores, thicker fibrous caps, and increased ratio of proresolving versus proinflammatory lipid mediators. These findings provide a plausible molecular-cellular mechanism that contributes to defective efferocytosis, plaque necrosis, and impaired resolution during the progression of atherosclerosis.

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Additional file 3 of Mer regulates microglial/macrophage M1/M2 polarization and alleviates neuroinflammation following traumatic brain injury
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Authors: Cai, B., Thorp, E. B., Doran, A. C., Sansbury, B. E., Daemen, M. J. A. P., Dorweiler, B., Spite, M., Fredman, G., & Tabas, I.
Affiliations: Columbia University (US)
Northwestern University (US)
Brigham and Women's Hospital (US)
Amsterdam UMC Location University of Amsterdam (NL)
Johannes Gutenberg University Mainz (DE)
Albany Medical College (US)
Corresponding author: Tabas, Ira
ORCID: Cai, Bishuang
Thorp, Edward B.
Doran, Amanda C.
Sansbury, Brian E.
Daemen, Mat J.A.P.
Dorweiler, Bernhard
Spite, Matthew
Fredman, Gabrielle
Tabas, Ira
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2017-01-09
Volume: 127
Issue: 2
Pages: 564-568
ISSN: 0021-9738 (ISSN-L)
1558-8238
DOI: 10.1172/jci90520
PMC: PMC5272169
OpenAlex: W2569227792
Cited by: 262
References: 39
Citations by year: 2026: 37 · 2025: 34 · 2024: 38 · 2023: 27 · 2022: 23 · 2021: 28 · 2020: 18 · 2019: 21 · 2018: 19 · 2017: 16
FWCI: 9.16
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Pure Amsterdam UMC (publishedVersion, other-oa)
Data Archiving and Networked Services (DANS) (submittedVersion)
Figshare (submittedVersion, cc-by)
Health Research Alliance (cc-by)
Funders: American Heart Association (T32 HL007854)
National Institutes of Health (UL1TR001422, HL119587, HL007854)
National Heart, Lung, and Blood Institute (R01HL122309, R01HL132412, R01HL140554, R01HL127464, R00HL119587, K99HL119587, P01HL087123, R01HL075662, R01HL106173, T32HL007854)
National Institute of General Medical Sciences (P01GM095467)
National Center for Advancing Translational Sciences
Topics: Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
Keywords: MERTK, efferocytosis, plaque necrosis, atherosclerosis, inflammation resolution, macrophages, necrotic core, fibrous cap, carotid plaque, specialized pro-resolving mediators, Ldlr-deficient mice, atherothrombosis
MeSH terms: c-Mer Tyrosine Kinase, Animals, Carotid Artery Diseases, Female, Humans, Male, Necrosis, Proto-Oncogene Proteins, Receptors, LDL, Mice, Knockout, Receptor Protein-Tyrosine Kinases, Mice, Plaque, Atherosclerotic, Proteolysis

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

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MerTK receptor cleavage promotes plaque necrosis and defective resolution in atherosclerosis

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