-
1دورية أكاديمية
المؤلفون: Xi Xu, Xiao-Dan Xu, Meng-Qing Ma, Yin Liang, Yang-Bo Cai, Zi-Xian Zhu, Tao Xu, Lin Zhu, Kun Ren
المصدر: Biomedicine & Pharmacotherapy, Vol 171, Iss , Pp 116112- (2024)
مصطلحات موضوعية: Ferroptosis, Reactive oxygen species, Lipid peroxidation, Plaque cells, Atherosclerosis, Therapeutics. Pharmacology, RM1-950
الوصف: Ferroptosis is a newly identified form of non-apoptotic programmed cell death, characterized by the iron-dependent accumulation of lethal lipid reactive oxygen species (ROS) and peroxidation of membrane polyunsaturated fatty acid phospholipids (PUFA-PLs). Ferroptosis is unique among other cell death modalities in many aspects. It is initiated by excessive oxidative damage due to iron overload and lipid peroxidation and compromised antioxidant defense systems, including the system Xc-/ glutathione (GSH)/glutathione peroxidase 4 (GPX4) pathway and the GPX4-independent pathways. In the past ten years, ferroptosis was reported to play a critical role in the pathogenesis of various cardiovascular diseases, e.g., atherosclerosis (AS), arrhythmia, heart failure, diabetic cardiomyopathy, and myocardial ischemia-reperfusion injury. Studies have identified dysfunctional iron metabolism and abnormal expression profiles of ferroptosis-related factors, including iron, GSH, GPX4, ferroportin (FPN), and SLC7A11 (xCT), as critical indicators for atherogenesis. Moreover, ferroptosis in plaque cells, i.e., vascular endothelial cell (VEC), macrophage, and vascular smooth muscle cell (VSMC), positively correlate with atherosclerotic plaque development. Many macromolecules, drugs, Chinese herbs, and food extracts can inhibit the atherogenic process by suppressing the ferroptosis of plaque cells. In contrast, some ferroptosis inducers have significant pro-atherogenic effects. However, the mechanisms through which ferroptosis affects the progression of AS still need to be well-known. This review summarizes the molecular mechanisms of ferroptosis and their emerging role in AS, aimed at providing novel, promising druggable targets for anti-AS therapy.
وصف الملف: electronic resource
العلاقة: http://www.sciencedirect.com/science/article/pii/S0753332223019108Test; https://doaj.org/toc/0753-3322Test
-
2دورية أكاديمية
المؤلفون: Michele F. Buono, Ernest Diez Benavente, Lotte Slenders, Daisey Methorst, Daniëlle Tessels, Eloi Mili, Roxy Finger, Daniek Kapteijn, Mark Daniels, Noortje A. M. van den Dungen, Jorg J. A. Calis, Barend M. Mol, Gert J. de Borst, Dominique P. V. de Kleijn, Gerard Pasterkamp, Hester M. den Ruijter, Michal Mokry
المصدر: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, Vol 12, Iss 21 (2023)
مصطلحات موضوعية: disease modeling, myofibroblast, phenotypic modulation, plaque cells, smooth muscle cell, Diseases of the circulatory (Cardiovascular) system, RC666-701
الوصف: Background Plaque myofibroblasts are critical players in the initiation and advancement of atherosclerotic disease. They are involved in the production of extracellular matrix, the formation of the fibrous cap, and the underlying lipidic core via modulation processes in response to different environmental cues. Despite clear phenotypic differences between myofibroblast cells and healthy vascular smooth muscle cells, smooth muscle cells are still widely used as a cellular model in atherosclerotic research. Methods and Results Here, we present a conditioned outgrowth method to isolate and culture myofibroblast cells from plaques. We obtained these cells from 27 donors (24 carotid and 3 femoral endarterectomies). We show that they keep their proliferative capacity for 8 passages, are transcriptionally stable, retain donor‐specific gene expression programs, and express extracellular matrix proteins (FN1, COL1A1, and DCN) and smooth muscle cell markers (ACTA2, MYH11, and CNN1). Single‐cell transcriptomics reveals that the cells in culture closely resemble the plaque myofibroblasts. Chromatin immunoprecipitation sequencing shows the presence of histone H3 lysine 4 dimethylation at the MYH11 promoter, pointing to their smooth muscle cell origin. Finally, we demonstrated that plaque myofibroblasts can be efficiently transduced (>97%) and are capable of taking up oxidized low‐density lipoprotein and undergoing calcification. Conclusions In conclusion, we present a method to isolate and culture cells that retain plaque myofibroblast phenotypical and functional capabilities, making them a suitable in vitro model for studying selected mechanisms of atherosclerosis.
وصف الملف: electronic resource
العلاقة: https://doaj.org/toc/2047-9980Test
-
3دورية أكاديمية
المؤلفون: Buono, Michele F, Benavente, Ernest Diez, Slenders, Lotte, Methorst, Daisey, Tessels, Daniëlle, Mili, Eloi, Finger, Roxy, Kapteijn, Daniek, Daniels, Mark, van den Dungen, Noortje A M, Calis, Jorg J A, Mol, Barend M, de Borst, Gert J, de Kleijn, Dominique P V, Pasterkamp, Gerard, den Ruijter, Hester M, Mokry, Michal
المساهمون: Experimentele Afd. Cardiologie 1, CDL Onderzoek Pasterkamp, CDL Research analisten, Cancer, Immuno/reuma onderzoek 1 (Vastert), Zorgeenheid Vaatchirurgie Medisch, Circulatory Health, Regenerative Medicine and Stem Cells, Infection & Immunity, Centraal Diagnostisch Laboratorium, Onderzoek Vrouw Hart & Vaatziekten, Child Health
مصطلحات موضوعية: disease modeling, myofibroblast, phenotypic modulation, plaque cells, smooth muscle cell, Cardiology and Cardiovascular Medicine
الوصف: Background Plaque myofibroblasts are critical players in the initiation and advancement of atherosclerotic disease. They are involved in the production of extracellular matrix, the formation of the fibrous cap, and the underlying lipidic core via modulation processes in response to different environmental cues. Despite clear phenotypic differences between myofibroblast cells and healthy vascular smooth muscle cells, smooth muscle cells are still widely used as a cellular model in atherosclerotic research. Methods and Results Here, we present a conditioned outgrowth method to isolate and culture myofibroblast cells from plaques. We obtained these cells from 27 donors (24 carotid and 3 femoral endarterectomies). We show that they keep their proliferative capacity for 8 passages, are transcriptionally stable, retain donor-specific gene expression programs, and express extracellular matrix proteins (FN1, COL1A1, and DCN) and smooth muscle cell markers (ACTA2, MYH11, and CNN1). Single-cell transcriptomics reveals that the cells in culture closely resemble the plaque myofibroblasts. Chromatin immunoprecipitation sequencing shows the presence of histone H3 lysine 4 dimethylation at the MYH11 promoter, pointing to their smooth muscle cell origin. Finally, we demonstrated that plaque myofibroblasts can be efficiently transduced (>97%) and are capable of taking up oxidized low-density lipoprotein and undergoing calcification. Conclusions In conclusion, we present a method to isolate and culture cells that retain plaque myofibroblast phenotypical and functional capabilities, making them a suitable in vitro model for studying selected mechanisms of atherosclerosis.
وصف الملف: application/pdf
-
4دورية أكاديمية
المؤلفون: Buono, Michele F, Slenders, Lotte, Wesseling, Marian, Hartman, Robin J G, Monaco, Claudia, den Ruijter, Hester M, Pasterkamp, Gerard, Mokry, Michal
المساهمون: Experimentele Afd. Cardiologie 1, CDL Onderzoek Pasterkamp, Circulatory Health, Onderzoek Vrouw Hart & Vaatziekten, Centraal Diagnostisch Laboratorium, Child Health
مصطلحات موضوعية: Atherosclerotic plaque, Disease modelling, Phenotypic switch, Plaque cells, Vulnerable plaque, Journal Article, Review
الوصف: For decades, the pathological definition of the vulnerable plaque led to invaluable insights into the mechanisms that underlie myocardial infarction and stroke. Beyond plaque rupture, other mechanisms, such as erosion, may elicit thrombotic events underlining the complexity and diversity of the atherosclerotic disease. Novel insights, based on single-cell transcriptomics and other “omics” methods, provide tremendous opportunities in the ongoing search for cell-specific determinants that will fine-tune the description of the thrombosis prone lesion. It coincides with an increasing awareness that knowledge on lesion characteristics, cell plasticity and clinical presentation of ischemic cardiovascular events have shifted over the past decades. This shift correlates with an observed changes of cell composition towards phenotypical stabilizing of human plaques. These stabilization features and mechanisms are directly mediated by the cells present in plaques and can be mimicked in vitro via primary plaque cells derived from human atherosclerotic tissues.
وصف الملف: application/pdf
-
5
المؤلفون: Tatsuya Sawamura, Pierfrancesco Agostoni, Maurizio Anselmi, Ulisse Garbin, Luciano Cominacini, Cristina Nava, Dritan Keta, Pietro Zardini, Chiara Stranieri, Vincenzo Lo Cascio, Anna Fratta Pasini, Massimiliano Fusaro
المصدر: Journal of the American College of Cardiology. (5):799-806
مصطلحات موضوعية: Male, medicine.medical_specialty, Peripheral blood mononuclear cell, LDL, Angina, chemistry.chemical_compound, ACUTE CORONARY SYNDROMES, SCAVENGER RECEPTORS, ARTERY-DISEASE, LDL, ATHEROSCLEROSIS, PLAQUE, CELLS, Internal medicine, medicine, Humans, ARTERY-DISEASE, Angina, Unstable, Scavenger receptor, Receptor, Aged, SCAVENGER RECEPTORS, Unstable angina, Cholesterol, business.industry, ACUTE CORONARY SYNDROMES, Case-control study, NF-kappa B, Cholesterol, LDL, Middle Aged, medicine.disease, PLAQUE, Lipoproteins, LDL, Receptors, Oxidized LDL, Endocrinology, chemistry, ATHEROSCLEROSIS, Case-Control Studies, CELLS, Female, business, Cardiology and Cardiovascular Medicine, Lipoprotein
الوصف: ObjectivesThe purpose of this study was to investigate the effect of circulating levels of oxidized low-density lipoprotein (ox-LDL) on nuclear factor-kappa B (NF-kB) activation in peripheral blood mononuclear cells (PBMC) of patients with unstable angina (UA) or stable angina (SA) and control subjects.BackgroundNuclear factor-kB might be involved in atherosclerosis, as is suggested by the presence of activated NF-kB in human atherosclerotic lesions.MethodsLevels of plasma ox-LDL and circulating NF-kB in PBMC (and in separated lymphocytes and monocytes) were measured in 27 control subjects and 29 SA and 27 UA patients. In in vitro studies, the effect of ox-LDL and of the sera derived from a subgroup of UA patients and control subjects on monocytic NF-kB activation was also evaluated.ResultsThe UA and SA patients had higher levels of circulating ox-LDL and NF-kB in PBMC than control subjects (p < 0.001). The increase in circulating NF-kB was mainly due to the activation of monocytes. In the in vitro studies, ox-LDL dose-dependently increased the activation of NF-kB in monocytes, but not in lymphocytes derived from healthy volunteers. This increase was related to the expression of lectin-like ox-LDL receptor-1 on monocytes. The incubation of monocytes with the sera derived from the UA patients induced a significant increase in NF-kB activation compared with the sera derived from the control subjects.ConclusionsThe data suggest that the activation of NF-kB in monocytes of UA patients is, at least in part, induced by circulating molecules such as ox-LDL, which has been found to be particularly elevated in UA patients.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0bc66a05c940d17ae2e4453be6892bb1Test
-
6
-
7مورد إلكتروني
المؤلفون: Tessels, Daniëlle
مصطلحات الفهرس: Atherosclerosis is a chronic inflammatory condition which results in the formation of atherosclerotic plaques. Foam cells play an important role in the development of the atherosclerotic plaque by forming the lipid core. It is known that macrophages and smooth muscle cells have the ability to take up oxidised low-density lipoprotein and thereby become foam cells. However, it is not known if transdifferentiated smooth muscle cells in the plaque, also called plaque cells, can also become foam cell, Master Thesis, Student Thesis
النص الكامل