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https://www.readbyqxmd.com/read/29684642/innate-and-adaptive-immunity-in-atherosclerosis
#1
REVIEW
Kapka Miteva, Rosalinda Madonna, Raffaele De Caterina, Sophie Van Linthout
Atherosclerosis is a chronic inflammatory disorder of the large and medium-size arteries characterized by the subendothelial accumulation of cholesterol, immune cells, and extracellular matrix. At the early onset of atherogenesis, endothelial dysfunction takes place. Atherogenesis is further triggered by the accumulation of cholesterol-carrying low-density lipoproteins, which acquire properties of damage-associated molecular patterns and thereby trigger an inflammatory response. Following activation of the innate immune response, mainly governed by monocytes and macrophages, the adaptive immune response is started which further promotes atherosclerotic plaque formation...
April 20, 2018: Vascular Pharmacology
https://www.readbyqxmd.com/read/29681573/amlodipine-inhibits-vascular-cell-senescence-and-protects-against-atherogenesis-through-the-mechanism-independent-of-calcium-channel-blockade
#2
Hiromi Kayamori, Ippei Shimizu, Yohko Yoshida, Yuka Hayashi, Masayoshi Suda, Ryutaro Ikegami, Goro Katsuumi, Takayuki Wakasugi, Tohru Minamino
Vascular cells have a finite lifespan and eventually enter irreversible growth arrest called cellular senescence. We have previously suggested that vascular cell senescence contributes to the pathogenesis of human atherosclerosis. Amlodipine is a mixture of two enantiomers, one of which (S- enantiomer) has L-type channel blocking activity, while the other (R+ enantiomer) shows ~1000-fold weaker channel blocking activity than S- enantiomer and has other unknown effects. It has been reported that amlodipine inhibits the progression of atherosclerosis in humans, but the molecular mechanism of this beneficial effect remains unknown...
April 20, 2018: International Heart Journal
https://www.readbyqxmd.com/read/29674474/genetic-deletion-of-il-interleukin-19-exacerbates-atherogenesis-in-il19-%C3%A3-ldlr-double-knockout-mice-by-dysregulation-of-mrna-stability-protein-hur-human-antigen-r
#3
Mitali Ray, Khatuna Gabunia, Christine N Vrakas, Allison B Herman, Farah Kako, Sheri E Kelemen, Laurel A Grisanti, Michael V Autieri
OBJECTIVE: To test the hypothesis that loss of IL (interleukin)-19 exacerbates atherosclerosis. APPROACH AND RESULTS: Il19 -/- mice were crossed into Ldlr -/- (low-density lipoprotein receptor knock out) mice. Double knockout (dKO) mice had increased plaque burden in aortic arch and root compared with Ldlr -/- controls after 14 weeks of high-fat diet (HFD). dKO mice injected with 10 ng/g per day rmIL-19 had significantly less plaque compared with controls. qRT-PCR and Western blot analysis revealed dKO mice had increased systemic and intraplaque polarization of T cells and macrophages to proinflammatory Th 1 and M1 phenotypes, and also significantly increased TNF (tumor necrosis factor)-α expression in spleen and aortic arch compared with Ldlr -/- controls...
April 19, 2018: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/29673358/contribution-of-tlr4-signaling-in-intermittent-hypoxia-mediated-atherosclerosis-progression
#4
Xianqin Zeng, Rong Guo, Mei Dong, Julia Zheng, Huili Lin, Huixia Lu
BACKGROUND: Intermittent hypoxia (IH), a typical character of obstructive sleep apnea (OSA), is related to atherogenesis. However, the role of IH on atherosclerosis (AS) progression and the mechanisms involved remains poorly understood. METHODS: In the present study, high-fat fed ApoE-/- mice were treated with recombinant shRNA-TLR4 lentivirus and exposed to IH. Atherosclerotic lesions on the en face aorta and cross-sections of aortic root were examined by Oil-Red O staining...
April 19, 2018: Journal of Translational Medicine
https://www.readbyqxmd.com/read/29669944/neutrophil-subsets-and-their-gene-signature-associate-with-vascular-inflammation-and-coronary-atherosclerosis-in-lupus
#5
Philip M Carlucci, Monica M Purmalek, Amit K Dey, Yenealem Temesgen-Oyelakin, Simantini Sakhardande, Aditya A Joshi, Joseph B Lerman, Alice Fike, Michael Davis, Jonathan H Chung, Martin P Playford, Mohammad Naqi, Pragnesh Mistry, Gustavo Gutierrez-Cruz, Stefania Dell'Orso, Faiza Naz, Taufiq Salahuddin, Balaji Natarajan, Zerai Manna, Wanxia L Tsai, Sarthak Gupta, Peter Grayson, Heather Teague, Marcus Y Chen, Hong-Wei Sun, Sarfaraz Hasni, Nehal N Mehta, Mariana J Kaplan
BACKGROUND: Systemic lupus erythematosus (SLE) is associated with enhanced risk of atherosclerotic cardiovascular disease not explained by Framingham risk score (FRS). Immune dysregulation associated to a distinct subset of lupus proinflammatory neutrophils (low density granulocytes; LDGs) may play key roles in conferring enhanced CV risk. This study assessed if lupus LDGs are associated with in vivo vascular dysfunction and inflammation and coronary plaque. METHODS: SLE subjects and healthy controls underwent multimodal phenotyping of vascular disease by quantifying vascular inflammation (18F-fluorodeoxyglucose-PET/CT [18F-FDG-PET/CT]), arterial dysfunction (EndoPAT and cardio-ankle vascular index), and coronary plaque burden (coronary CT angiography)...
April 19, 2018: JCI Insight
https://www.readbyqxmd.com/read/29663503/mir-135a-represses-oxidative-stress-and-vascular-inflammatory-events-via-targeting-toll-like-receptor-4-in-atherogenesis
#6
Xian-Jin Du, Jing-Min Lu
Plenty of microRNAs have been identified as critical mediators in atherosclerosis progression, which is still a great threat to human health. Oxidative stress and inflammation have been implicated to contribute a lot to atherosclerosis development. MiR-135a is abnormally expressed in various cancer types, however its function in atherosclerosis is largely unexplored. Ox-LDL is commonly recognized as a crucial atherosclerosis regulator. In our current study, we observed ox-LDL was able to induce RAW264.7 cell apoptosis and meanwhile miR-135a was restrained by ox-LDL both dose-dependently and time- dependently...
April 16, 2018: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/29662563/-123-i-labeled-oxldl-is-widely-distributed-throughout-the-whole-body-in-mice
#7
Atushi Nakano, Hidekazu Kawashima, Yoshinori Miyake, Tsutomu Zeniya, Akihide Yamamoto, Kazuhiro Koshino, Takashi Temma, Tetsuya Fukuda, Yoshiko Fujita, Akemi Kakino, Shigehiko Kanaya, Tatsuya Sawamura, Hidehiro Iida
Purpose: Oxidized low-density lipoprotein (oxLDL) plays a key role in endothelial dysfunction, vascular inflammation, and atherogenesis. The aim of this study was to assess blood clearance and in vivo kinetics of radiolabeled oxLDL in mice. Methods: We synthesized 123 I-oxLDL by the iodine monochloride method, and performed an uptake study in CHO cells transfected with lectin-like oxLDL receptor-1 (LOX-1). In addition, we evaluated the consistency between the 123 I-oxLDL autoradiogram and the fluorescence image of DiI-oxLDL after intravenous injection for both spleen and liver...
April 2018: Nuclear Medicine and Molecular Imaging
https://www.readbyqxmd.com/read/29659956/polyphenols-have-no-impact-on-endothelial-function-in-patients-with-obstructive-sleep-apnea-a-randomized-controlled-trial
#8
Wojciech Trzepizur, Vanessa Bironneau, Sylvain Recoquillon, Pascaline Priou, Nicole Meslier, Jean-François Hamel, Samir Henni, Astrid Darsonval, Khaled Messaoudi, Maria Carmen Martínez, Ramaroson Andriantsitohaina, Frédéric Gagnadoux
Background: Endothelial dysfunction, a pathophysiologic determinant of atherogenesis, has been found to occur in obstructive sleep apnea syndrome (OSA) and is improved by continuous positive airway pressure (CPAP). However, the efficacy of CPAP therapy is limited by variable adherence. Alternative treatment strategies are needed. The impact of polyphenols on endothelial function has never been evaluated in OSA. Objective: We evaluated the impact of 1-mo supplementation with grape juice polyphenols (GJPs) on the reactive hyperemia index (RHI), a validated measure of endothelial function in patients with severe OSA...
April 1, 2018: Journal of Nutrition
https://www.readbyqxmd.com/read/29658969/combined-gstm1-and-gstt1-null-genotypes-are-strong-risk-factors-for-atherogenesis-in-a-serbian-population
#9
Ivana Grubisa, Petar Otasevic, Nada Vucinic, Biljana Milicic, Tanja Jozic, Slobodan Krstic, Jelena Milasin
Oxidative stress (OS) plays an important role in atherogenesis and since glutathione S-transferases (GSTs) provide protection against OS, we have tested the hypothesis that deletion polymorphisms in two GSTs (GSTM1 and GSTT1) may affect the risk of developing atherosclerosis. A total of 382 individuals (200 patients with atherosclerosis and 182 healthy controls) were included in this association study. Genomic DNA was isolated from peripheral blood cells or from buccal epithelial cells and genotyping was performed using multiplex-PCR or real-time PCR methods...
January 2018: Genetics and Molecular Biology
https://www.readbyqxmd.com/read/29656494/oxidized-ldl-phagocytosis-during-foam-cell-formation-in-atherosclerotic-plaques-relies-on-a-pld2-cd36-functional-interdependence
#10
Ramya Ganesan, Karen M Henkels, Lucile E Wrenshall, Yasunori Kanaho, Gilbert Di Paolo, Michael A Frohman, Julian Gomez-Cambronero
The uptake of cholesterol carried by low-density lipoprotein (LDL) is tightly controlled in the body. Macrophages are not well suited to counteract the cellular consequences of excess cholesterol leading to their transformation into "foam cells," an early step in vascular plaque formation. We have uncovered and characterized a novel mechanism involving phospholipase D (PLD) in foam cell formation. Utilizing bone marrow-derived macrophages from genetically PLD deficient mice, we demonstrate that PLD2 (but not PLD1)-null macrophages cannot fully phagocytose aggregated oxidized LDL (Agg-Ox-LDL), which was phenocopied with a PLD2-selective inhibitor...
April 14, 2018: Journal of Leukocyte Biology
https://www.readbyqxmd.com/read/29622164/tlr4-in-atherogenesis-paying-the-toll-for-antimicrobial-defense
#11
EDITORIAL
José J Fuster
No abstract text is available yet for this article.
April 10, 2018: Journal of the American College of Cardiology
https://www.readbyqxmd.com/read/29622163/chlamydia-and-lipids-engage-a-common-signaling-pathway-that-promotes-atherogenesis
#12
Shuang Chen, Kenichi Shimada, Timothy R Crother, Ebru Erbay, Prediman K Shah, Moshe Arditi
BACKGROUND: Recent studies indicate that Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88) signaling promote the development of high fat diet-induced atherosclerosis in hypercholesterolemic mice. OBJECTIVES: The authors investigated the role of TLR4/MyD88 signaling in hematopoietic and stromal cells in the development and infection-mediated acceleration of atherosclerosis. METHODS: The authors generated bone marrow chimeras between wild-type and Tlr4-/- mice, as well as wild-type and Myd88-/- mice...
April 10, 2018: Journal of the American College of Cardiology
https://www.readbyqxmd.com/read/29617722/pcsk9-regulates-expression-of-scavenger-receptors-and-ox-ldl-uptake-in-macrophages
#13
Zufeng Ding, Shijie Liu, Xianwei Wang, Sue Theus, Xiaoyan Deng, Yubo Fan, Sichang Zhou, Jawahar L Mehta
Aims: PCSK9 has been shown to influence macrophage biology and modulate atherogenesis. We conducted this study to examine the regulation of scavenger receptors (SRs) (LOX-1, SRA and CD36) and oxidized liporoptein cholesterol (ox-LDL) uptake in macrophages by PCSK9. Methods and Results: Treatment of mouse peritoneal macrophages with TNF-α resulted in concentration-dependent modest, but significant, increase in PCSK9 expression. Importantly, treatment of TNF-α primed macrophages with recombinant murine PCSK9 increased the expression of LOX-1, SRA and CD36 2-5 fold, and enhanced ox-LDL uptake by ≈5-fold...
March 29, 2018: Cardiovascular Research
https://www.readbyqxmd.com/read/29614967/cardiovascular-outcomes-of-nephrotic-syndrome-in-childhood-cvons-study-a-protocol-for-prospective-cohort-study
#14
S K Patnaik, P Kumar, M Bamal, S Patel, M P Yadav, V Kumar, A Sinha, A Bagga, M Kanitkar
BACKGROUND: Nephrotic syndrome (NS) is characterized by dyslipidemia which is a well-known risk factor for atherogenesis. Atherosclerosis in childhood is mostly subclinical and endothelial dysfunction is known to precede this. Evidence for screening for endothelial dysfunction and cardiovascular risk factors and early identification of premature onset of atherosclerosis in childhood NS remains tenuous in the absence of well-designed prospective studies addressing cardiovascular comorbidity in NS...
April 3, 2018: BMC Nephrology
https://www.readbyqxmd.com/read/29601312/myeloid-cells-regulate-plasma-ldl-cholesterol-levels
#15
Venetia Bazioti, Anouk M La Rose, Marit Westerterp
PURPOSE OF REVIEW: Leukocytosis, elevated blood leukocyte levels, is associated with enhanced cardiovascular risk in humans. Hematopoietic stem and progenitor cells (HSPCs) drive leukocyte production in a process called hematopoiesis, which mainly occurs in the bone marrow, and under certain conditions also in other organs such as the spleen. Cholesterol accumulation in HSPCs enhances hematopoiesis, increasing levels of blood monocytes that infiltrate into atherosclerotic plaques. Although HSPC proliferation and monocytosis enhance atherogenesis in several studies, concomitant decreases in LDL-cholesterol levels have also been reported, associated with anti-atherogenic effects...
March 29, 2018: Current Opinion in Lipidology
https://www.readbyqxmd.com/read/29600751/electronegative-ldl-an-active-player-in-atherogenesis-or-a-by-product-of-atherosclerosis
#16
Andrea Rivas-Urbina, Anna Rull, Jordi Ordonez-Llanos, Jose Luis Sanchez-Quesada
Low-density lipoproteins (LDLs) are the major plasma carriers of cholesterol. However, LDL particles must undergo various molecular modifications to promote the development of atherosclerotic lesions. Modified LDL can be generated by different mechanisms, but as a common trait, show an increased electronegative charge of the LDL particle. A subfraction of LDL with increased electronegative charge (LDL(-)), which can be isolated from blood, exhibits several pro-atherogenic characteristics. LDL(-) is heterogeneous, due to its multiple origins but is strongly related to the development of atherosclerosis...
March 29, 2018: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/29599138/telomerase-mediates-lymphocyte-proliferation-but-not-the-atherosclerosis-suppressive-potential-of-regulatory-t-cells
#17
Gavin Richardson, Andrew Sage, Karim Bennaceur, Nayef Al Zhrany, Jose Coelho-Lima, Emily Dookun, Lilia Draganova, Gabriele Saretzki, David T Breault, Ziad Mallat, Ioakim Spyridopoulos
OBJECTIVE: Atherosclerosis is an age-related disease characterized by systemic oxidative stress and low-grade inflammation. The role of telomerase and telomere length in atherogenesis remains contentious. Short telomeres of peripheral leukocytes are predictive for coronary artery disease. Conversely, attenuated telomerase has been demonstrated to be protective for atherosclerosis. Hence, a potential causative role of telomerase in atherogenesis is critically debated. APPROACH AND RESULTS: In this study, we used multiple mouse models to investigate the regulation of telomerase under oxidative stress as well as its impact on atherogenesis in vitro and in vivo...
March 29, 2018: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/29598451/novel-drug-discovery-strategies-for-atherosclerosis-that-target-necrosis-and-necroptosis
#18
Isabelle Coornaert, Sam Hofmans, Lars Devisscher, Koen Augustyns, Pieter Van Der Veken, Guido R Y De Meyer, Wim Martinet
Formation and enlargement of a necrotic core play a pivotal role in atherogenesis. Since the discovery of necroptosis, which is a regulated form of necrosis, prevention of necrotic cell death has become an attractive therapeutic goal to reduce plaque formation. Areas covered: This review highlights the triggers and consequences of (unregulated) necrosis and necroptosis in atherosclerosis. The authors discuss different pharmacological strategies to inhibit necrotic cell death in advanced atherosclerotic plaques...
March 29, 2018: Expert Opinion on Drug Discovery
https://www.readbyqxmd.com/read/29593789/drugs-involved-in-dyslipidemia-and-obesity-treatment-focus-on-adipose-tissue
#19
REVIEW
Sofia Dias, Sílvia Paredes, Laura Ribeiro
Metabolic syndrome can be defined as a state of disturbed metabolic homeostasis characterized by visceral obesity, atherogenic dyslipidemia, arterial hypertension, and insulin resistance. The growing prevalence of metabolic syndrome will certainly contribute to the burden of cardiovascular disease. Obesity and dyslipidemia are main features of metabolic syndrome, and both can present with adipose tissue dysfunction, involved in the pathogenic mechanisms underlying this syndrome. We revised the effects, and underlying mechanisms, of the current approved drugs for dyslipidemia and obesity (fibrates, statins, niacin, resins, ezetimibe, and orlistat; sibutramine; and diethylpropion, phentermine/topiramate, bupropion and naltrexone, and liraglutide) on adipose tissue...
2018: International Journal of Endocrinology
https://www.readbyqxmd.com/read/29589525/impact-of-dysfunctional-protein-catabolism-on-macrophage-cholesterol-handling
#20
Takuro Miyazaki, Akira Miyazaki
Protein catabolism in macrophages, which is accomplished mainly through autophagy-lysosomal degradation, ubiquitin-proteasome system, and calpains, is disturbed in atheroprone vessels. Moreover, growing evidence suggests that defects in protein catabolism interfere with cholesterol handling in macrophages. Indeed, decreases in autophagy facilitate the deposition of cholesterol in atheroprone macrophages and the subsequent development of vulnerable atherosclerotic plaques due to impaired catabolism of lipid droplets and limited efferocytic clearance of deadly cells...
March 26, 2018: Current Medicinal Chemistry
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