ArticleThe Journal of clinical investigation2008
Phospholipase C beta3 deficiency leads to macrophage hypersensitivity to apoptotic induction and reduction of atherosclerosis in mice.
Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Discovery of rare variants associated with blood pressure regulation through meta-analysis of 1.3 million individuals.Nature genetics · 2020Pooled it
- Phospholipase C epsilon 1 as a therapeutic target in cardiovascular diseases.Journal of advanced research · 2025Review
- Mammalian PI-Phospholipase C Isozymes: Structural and Functional Insights and Roles in Health and Disease.Medicina (Kaunas, Lithuania) · 2025Review
- Activation Mechanisms and Diverse Functions of Mammalian Phospholipase C.Biomolecules · 2023Review
- Cryptic mutations of PLC family members in brain disorders: recent discoveries and a deep-learning-based approach.Brain : a journal of neurology · 2023Review
- The Immunogenetics of Granulomatous Diseases.Advances in experimental medicine and biology · 2022Article
- Urinary Proteomics Identifying Novel Biomarkers for the Diagnosis and Phenotyping of Carotid Artery Stenosis.Frontiers in molecular biosciences · 2021Article
- Review
- Small GTPase ARF6 Is a Coincidence-Detection Code for RPH3A Polarization in Neutrophil Polarization.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Leukocyte Cytoskeleton Polarization Is Initiated by Plasma Membrane Curvature from Cell Attachment.Developmental cell · 2019Article
- Regulator of G protein signaling 5 restricts neutrophil chemotaxis and trafficking.The Journal of biological chemistry · 2018Article
- A membrane-associated, fluorogenic reporter for mammalian phospholipase C isozymes.The Journal of biological chemistry · 2018Article
- The macrophage C-type lectin receptor CLEC5A (MDL-1) expression is associated with early plaque progression and promotes macrophage survival.Journal of translational medicine · 2017Article
- Macrophages and Phospholipases at the Intersection between Inflammation and the Pathogenesis of HIV-1 Infection.International journal of molecular sciences · 2017Review
- PKN1 Directs Polarized RAB21 Vesicle Trafficking via RPH3A and Is Important for Neutrophil Adhesion and Ischemia-Reperfusion Injury.Cell reports · 2017Article
- Modulating Oxysterol Sensing to Control Macrophage Apoptosis and Atherosclerosis.Circulation research · 2016Article
- Nuclear factor-κB regulates expression of platelet phospholipase C-β2 (PLCB2).Thrombosis and haemostasis · 2016Article
- The Complement System Component C5a Produces Thermal Hyperalgesia via Macrophage-to-Nociceptor Signaling That Requires NGF and TRPV1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Phosphoinositide-specific phospholipase C in health and disease.Journal of lipid research · 2015Review
- Front-signal-dependent accumulation of the RHOA inhibitor FAM65B at leading edges polarizes neutrophils.Journal of cell science · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Atherosclerosis is an inflammatory disease that is associated with monocyte recruitment and subsequent differentiation into lipid-laden macrophages at sites of arterial lesions, leading to the development of atherosclerotic plaques. PLC is a key member of signaling pathways initiated by G protein-coupled ligands in macrophages. However, the role of this enzyme in the regulation of macrophage function is not known. Here, we studied macrophages from mice lacking PLC beta2, PLC beta3, or both PLC isoforms and found that PLC beta3 is the major functional PLC beta isoform in murine macrophages. Although PLC beta3 deficiency did not affect macrophage migration, adhesion, or phagocytosis, it resulted in macrophage hypersensitivity to multiple inducers of apoptosis. PLC beta3 appeared to regulate this sensitivity via PKC-dependent upregulation of Bcl-XL. The significance of PLC beta signaling in vivo was examined using the apoE-deficient mouse model of atherosclerosis. Mice lacking both PLC beta3 and apoE exhibited fewer total macrophages and increased macrophage apoptosis in atherosclerotic lesions, as well as reduced atherosclerotic lesion size when compared with mice lacking only apoE. These results demonstrate what we believe to be a novel role for PLC activity in promoting macrophage survival in atherosclerotic plaques and identify PLC beta3 as a potential target for treatment of atherosclerosis.
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What OpenQuestion holds
Registered trials
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.