Cited by 967Phagocytosis and Immune RegulationCell death mechanisms and regulationAutophagy in Disease and Therapy

Apoptotic Cells Induce Migration of Phagocytes via Caspase-3-Mediated Release of a Lipid Attraction Signal

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Lauber, Kirsten, Bohn, Erwin, Kröber, Stefan Martin, Xiao, Yi-jin, Blumenthal, Sibylle G., Lindemann, Ralph K., Marini, Patrizia, Wiedig, Carolin +8 more·2003·Cell

Abstract

Efficient engulfment of the intact cell corpse is a critical end point of apoptosis, required to prevent secondary necrosis and inflammation. The presentation of "eat-me" signals on the dying cell is an important part of this process of recognition and engulfment by professional phagocytes. Here, we present evidence that apoptotic cells secrete chemotactic factor(s) that stimulate the attraction of monocytic cells and primary macrophages. The activation of caspase-3 in the apoptotic cell was found to be required for the release of this chemotactic factor(s). The putative chemoattractant was identified as the phospholipid, lysophosphatidylcholine. Further analysis showed that lysophosphatidylcholine was released from apoptotic cells due to the caspase-3 mediated activation of the calcium-independent phospholipase A(2). These data suggest that in addition to eat-me signals, apoptotic cells display attraction signals to ensure the efficient removal of apoptotic cells and prevent postapoptotic necrosis.

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Registry

Crossref · 10.1016/s0092-8674(03)00422-7

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35 of 35 references verified0 citation errors · 0 not checkable

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  • Autoimmunity is observed in mice whose phagocytes lack G2A, a receptor required for response to lysophosphatidylcholine.

    “However, autoimmunity has been observed in mice in which phagocytes lack the G-protein coupled receptor G2A41, which is required for the response to lysophosphatidylcholine 42”

    From Immunogenic and tolerogenic cell death (2009) · cites this paper as [41]

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Authors
Lauber, K., Bohn, E., Kröber, S. M., Xiao, Y.-J., Blumenthal, S. G., Lindemann, R. K., Marini, P., Wiedig, C., Zobywalski, A., Baksh, S., Xu, Y., Autenrieth, I. B., Schulze-Osthoff, K., Belka, C., Stuhler, G., & Wesselborg, S.
Affiliations
  • University of Tübingen (DE)
  • Cleveland Clinic (US)
  • Beth Israel Deaconess Medical Center (US)
Corresponding author
Wesselborg, Sebastian
Venue
Cell
Publisher
Elsevier BV
Published
2003-06
Volume
113
Issue
6
Pages
717-730
ISSN
0092-8674 (ISSN-L)
OpenAlex
W2159330173
Cited by
967
References
35
Citations by year
2026: 31 · 2025: 31 · 2024: 42 · 2023: 41 · 2022: 50 · 2021: 40 · 2020: 32 · 2019: 31 · 2018: 43 · 2017: 33 · 2016: 37 · 2015: 39 · 2014: 44 · 2013: 43 · 2012: 36
FWCI
15.86
Type
journal article
Language
en
Open access
Locations
  • Cell (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
efferocytosis, caspase-3, lysophosphatidylcholine, phagocyte migration, macrophages, monocytic cells, calcium-independent phospholipase A2, eat-me signals, secondary necrosis, inflammation
MeSH terms
Animals, Chemotaxis, Enzyme Inhibitors, Eukaryotic Cells, Humans, Inflammation, Lysophosphatidylcholines, Phagocytes, Phagocytosis, Phospholipases A, Protein Synthesis Inhibitors, Signal Transduction, Ankyrin Repeat, Apoptosis, HT29 Cells, COS Cells, Caspases, Cell Surface Extensions, Lipid Metabolism, Mice, Caspase 3

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