ArticleLaboratory investigation; a journal of technical methods and pathology2019
Characterization of smooth muscle cells from human atherosclerotic lesions and their responses to Notch signaling.
Article in Laboratory investigation; a journal of technical methods and pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Extreme Diversity of the Human Vascular Mesenchymal Cell Landscape.Journal of the American Heart Association · 2020Pooled it
- Why Are Internal Mammary (Thoracic) Arteries Less Prone to Developing Atherosclerosis Compared to Coronary Arteries? Do Gut Microbiota Play a Role? A Narrative Review.International journal of molecular sciences · 2025Review
- CADASIL orFrontiers in neurology · 2025Review
- Plasma NOTCH3 and the risk of cardiovascular recurrence in patients with ischemic stroke.QJM : monthly journal of the Association of Physicians · 2024Article
- CircLZIC regulates ox-LDL-induced HUVEC cell proliferation and apoptosis via Micro-330-5p/NOTCH2 axis in atherosclerosis.Clinical hemorheology and microcirculation · 2024Article
- Purification of functional mouse skeletal muscle mitochondria using percoll density gradient centrifugation.BMC research notes · 2023Article
- Caveolin-1 inhibition mediates the opposing effects of alcohol on γ-secretase activity in arterial endothelial and smooth muscle cells.Physiological reports · 2023Article
- Biomedical engineering approaches for the delivery of JAGGED1 as a potential tissue regenerative therapy.Frontiers in bioengineering and biotechnology · 2023Review
- Preventing Cholesterol-Induced Perk (Protein Kinase RNA-Like Endoplasmic Reticulum Kinase) Signaling in Smooth Muscle Cells Blocks Atherosclerotic Plaque Formation.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- NOTCH3 as a modulator of vascular disease: a target in elastin deficiency and arterial pathologies.The Journal of clinical investigation · 2022Article
- Article
- Smooth Muscle Cell Notch2 Is Not Required for Atherosclerotic Plaque Formation in ApoE Null Mice.Journal of vascular research · 2022Article
- Immobilization of Jagged1 Enhances Vascular Smooth Muscle Cells Maturation by Activating the Notch Pathway.Cells · 2021Article
- SVEP1 is a human coronary artery disease locus that promotes atherosclerosis.Science translational medicine · 2021Article
- Mural Cells: Potential Therapeutic Targets to Bridge Cardiovascular Disease and Neurodegeneration.Cells · 2021Review
- Analysis of Molecular Mechanism of YiqiChutan Formula Regulating DLL4-Notch Signaling to Inhibit Angiogenesis in Lung Cancer.BioMed research international · 2021Article
- Biological Significance of NOTCH Signaling Strength.Frontiers in cell and developmental biology · 2021Review
- Smooth muscle cells in atherosclerosis: clones but not carbon copies.JVS-vascular science · 2021Review
- The pathophysiological basis of vascular disease.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Notch2 and Proteomic Signatures in Mouse Neointimal Lesion Formation.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Atherosclerosis is the most common cause of heart disease and stroke. The use of animal models has advanced our understanding of the molecular signaling that contributes to atherosclerosis. Further understanding of this degenerative process in humans will require human tissue. Plaque removed during endarterectomy procedures to relieve arterial obstructions is usually discarded, but can be an important source of diseased cells. Resected tissue from carotid and femoral endarterectomy procedures were compared with carotid arteries from donors with no known cardiovascular disease. Vascular smooth muscle cells (SMC) contribute to plaque formation and may determine susceptibility to rupture. Notch signaling is implicated in the progression of atherosclerosis, and plays a receptor-specific regulatory role in SMC. We defined protein localization of Notch2 and Notch3 within medial and plaque SMC using immunostaining, and compared Notch2 and Notch3 levels in total plaques with whole normal arteries using immunoblot. We successfully derived SMC populations from multiple endarterectomy specimens for molecular analysis. To better define the protein signature of diseased SMC, we utilized sequential window acquisition of all theoretical spectra (SWATH) proteomic analysis to compare normal carotid artery SMC with endarterectomy-derived SMC. Similarities in protein profile and differentiation markers validated the SMC identity of our explants. We identified a subset of differentially expressed proteins that are candidates as functional markers of diseased SMC. To understand how Notch signaling may affect diseased SMC, we performed Jagged1 stimulation of primary cultures. In populations that displayed significant growth, Jagged1 signaling through Notch2 suppressed proliferation; cultures with low growth potential were non-responsive to Jagged1. In addition, Jagged1 did not promote contractile smooth muscle actin nor have a significant effect on the mature differentiated phenotype. Thus, SMC derived from atherosclerotic lesions show distinct proteomic profiles and have altered Notch signaling in response to Jagged1 as a differentiation stimulus, compared with normal SMC.
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Registered trials
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