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macrophage and atherogenesis

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https://www.readbyqxmd.com/read/27924297/datasets-for-the-validation-of-the-in-vivo-sirna-silencing-of-cd40-and-for-the-detection-of-new-markers-of-atherosclerosis-progression-in-apoe-deficient-mice
#1
Miguel Hueso, Laura De Ramon, Estanislao Navarro, Elia Ripoll, Josep M Cruzado, Josep M Grinyo, Joan Torras
Data presented in this Data in Brief article correspond to the article "in vivo" silencing of CD40 reduces progression of experimental atherogenesis through a NFκB/miR-125b axis and reveals new potential mediators in the pathogenesis of atherosclerosis" (M. Hueso, L. De Ramon, E. Navarro, E. Ripoll, J.M. Cruzado, J.M. Grinyo, J. Torras, 2016) [1]. Here, we describe the validation of the silencing of CD40 expression with a specific siRNA in ApoE(-/-) mouse aortas, and its systemic effects on splenic lymphocytic subpopulations as well as on the infiltration of aortic intima by F4/80(+), galectin-3(+) macrophages or by NF-κB(+) cells...
December 2016: Data in Brief
https://www.readbyqxmd.com/read/27910925/thrombomodulin-regulates-monocye-differentiation-via-pkc%C3%AE-and-erk1-2-pathway-in-vitro-and-in-atherosclerotic-artery
#2
Chien-Sung Tsai, Yi-Wen Lin, Chun-Yao Huang, Chun-Min Shih, Yi-Ting Tsai, Nai-Wen Tsao, Chin-Sheng Lin, Chun-Che Shih, Hellen Jeng, Feng-Yen Lin
Thrombomodulin (TM) modulates the activation of protein C and coagulation. Additionally, TM regulates monocyte migration and inflammation. However, its role on monocyte differentiation is still unknown. We investigated the effects of TM on monocyte differentiation. First, we found that TM was increased when THP-1 cells were treated with phorbol-12-myristate-13-acetate (PMA). Overexpression of TM enhanced the macrophage markers, CD14 and CD68 expression in PMA-induced THP-1. TM siRNA depressed the PMA-induced increase of p21(Cip1/WAF1) via ERK1/2-NF-kB p65 signaling...
December 2, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27871915/inhibition-of-siglec-1-by-lentivirus-mediated-small-interfering-rna-attenuates-atherogenesis-in-apoe-deficient-mice
#3
Yi-Song Xiong, Ai-Lin Wu, Dong Mu, Juan Yu, Ping Zeng, Yi Sun, Jie Xiong
BACKGROUND: Siglec-1 is highly expressed on circulating monocytes and plaque macrophages in atherosclerotic patients, but the exact role of Siglec-1 in atherosclerosis has not been elucidated. METHODS: Lentiviral vector containing small interfering RNA targeting Siglec-1 (Lv-shSiglec-1) or control vector (Lv-shNC) were injected intravenously into 6-week old Apoe(-/-) mice. Then onset of atherosclerosis was observed. RESULTS: Siglec-1 was highly expressed in aortic plaques and it can be down-regulated by Lv-shSiglec-1 injection...
November 15, 2016: Clinical Immunology: the Official Journal of the Clinical Immunology Society
https://www.readbyqxmd.com/read/27871059/selective-p38%C3%AE-map-kinase-mapk14-inhibition-in-enzymatically-modified-ldl-stimulated-human-monocytes-implications-for-atherosclerosis
#4
Fei Cheng, Laura Twardowski, Sarah Fehr, Christoph Aner, Elke Schaeffeler, Thomas Joos, Thomas Knorpp, Bernhard Dorweiler, Stefan Laufer, Matthias Schwab, Michael Torzewski
The first ATP-competitive p38α MAPK/MAPK14 inhibitor with excellent in vivo efficacy and selectivity, skepinone-L, is now available. We investigated the impact of selective p38α MAPK/MAPK14 inhibition on enzymatically modified LDL (eLDL) stimulated human monocytes with its implications for atherosclerosis. Among the different p38 MAPK isoforms, p38α/MAPK14 was the predominantly expressed and activated isoform in isolated human peripheral blood monocytes. Moreover, eLDL colocalized with macrophages positive for p38α MAPK/MAPK14 in human carotid endarterectomy specimens...
November 8, 2016: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/27869741/isoliquiritigenin-attenuates-atherogenesis-in-apolipoprotein-e-deficient-mice
#5
Fen Du, Quzhen Gesang, Jia Cao, Mei Qian, Li Ma, Dongfang Wu, Hong Yu
Isoliquiritigenin (ISL) exhibits antioxidation and anti-inflammation activity. We sought to investigate the effects and mechanism of ISL on the development of atherosclerotic lesions in apolipoprotein E-deficient (apoE(-/-)) mice. Firstly, we determined that ISL reduced the mRNA levels of inflammatory factors interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), and monocyte chemotactic protein-1 (MCP-1), while it increased the expression of several lipoprotein-related genes in peritoneal macrophages treated with lipopolysaccharide (LPS)...
November 18, 2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/27856455/map3k8-modulates-monocyte-state-and-atherogenesis-in-apoe-mice
#6
Carlos Sanz-Garcia, Ángela Sánchez, Constanza Contreras-Jurado, Carmela Cales, Cristina Barranquero, Marta Muñóz, Ramón Merino, Paula Escudero, Maria-Jesús Sanz, Jesús Osada, Ana Aranda, Susana Alemany
OBJECTIVE: Map3k8 (Cot/Tpl2) activates the MKK1/2-ERK1/2, MAPK pathway downstream from interleukin-1R, tumor necrosis factor-αR, NOD-2R, adiponectinR, and Toll-like receptors. Map3k8 plays a key role in innate and adaptive immunity and influences inflammatory processes by modulating the functions of different cell types. However, its role in atherogenesis remains unknown. In this study, we analyzed the role of this kinase in this pathology. APPROACH AND RESULTS: We show here that Map3k8 deficiency results in smaller numbers of Ly6C(high)CD11c(low) and Ly6C(low)CD11c(high) monocytes in ApoE(-)(/-) mice fed a high-fat diet (HFD)...
November 17, 2016: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/27847551/caspase-3-deletion-promotes-necrosis-in-atherosclerotic-plaques-of-apoe-knockout-mice
#7
Mandy O J Grootaert, Dorien M Schrijvers, Marthe Hermans, Viviane O Van Hoof, Guido R Y De Meyer, Wim Martinet
Apoptosis of macrophages and vascular smooth muscle cells (VSMCs) in advanced atherosclerotic plaques contributes to plaque progression and instability. Caspase-3, a key executioner protease in the apoptotic pathway, has been identified in human and mouse atherosclerotic plaques but its role in atherogenesis is not fully explored. We therefore investigated the impact of caspase-3 deletion on atherosclerosis by crossbreeding caspase-3 knockout (Casp3(-/-)) mice with apolipoprotein E knockout (ApoE(-/-)) mice...
2016: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/27843203/mir-155-regulated-inflammation-response-by-the-socs1-stat3-pdcd4-axis-in-atherogenesis
#8
Jinshan Ye, Ruiwei Guo, Yankun Shi, Feng Qi, Chuanming Guo, Lixia Yang
Inflammation response plays a critical role in all phases of atherosclerosis (AS). Increased evidence has demonstrated that miR-155 mediates inflammatory mediators in macrophages to promote plaque formation and rupture. However, the precise mechanism of miR-155 remains unclear in AS. Here, we also found that miR-155 and PDCD4 were elevated in the aortic tissue of atherosclerotic mice and ox-LDL treated RAW264.7 cells. Further studies showed that miR-155 not only directly inhibited SOCS1 expression, but also increased the expression of p-STAT and PDCD4, as well as the production of proinflammation mediators IL-6 and TNF-α...
2016: Mediators of Inflammation
https://www.readbyqxmd.com/read/27835742/silencing-of-cd40-in%C3%A2-vivo-reduces-progression-of-experimental-atherogenesis-through-an-nf-%C3%AE%C2%BAb-mir-125b-axis-and-reveals-new-potential-mediators-in-the-pathogenesis-of-atherosclerosis
#9
Miguel Hueso, Laura De Ramon, Estanislao Navarro, Elia Ripoll, Josep M Cruzado, Josep M Grinyo, Joan Torras
BACKGROUND AND AIMS: CD40/CD40L signaling exerts a critical role in the development of atherosclerosis, and microRNAs (miRNAs) are key regulators in vascular inflammation and plaque formation. In this work, we investigated mRNA/miRNA expression during progression of atherosclerotic lesions through CD40 silencing. METHODS: We silenced CD40 with a specific siRNA in ApoE(-/-) mice and compared expression of mRNA/miRNA in ascending aorta with scrambled treated mice...
November 2, 2016: Atherosclerosis
https://www.readbyqxmd.com/read/27834690/rac2-modulates-atherosclerotic-calcification-by-regulating-macrophage-interleukin-1%C3%AE-production
#10
Nicolle Ceneri, Lina Zhao, Bryan D Young, Abigail Healy, Suleyman Coskun, Hema Vasavada, Timur O Yarovinsky, Kenneth Ike, Ruggero Pardi, Lingfen Qin, Li Qin, George Tellides, Karen Hirschi, Judith Meadows, Robert Soufer, Hyung J Chun, Mehran Sadeghi, Jeffrey R Bender, Alan R Morrison
OBJECTIVE: The calcium composition of atherosclerotic plaque is thought to be associated with increased risk for cardiovascular events, but whether plaque calcium itself is predictive of worsening clinical outcomes remains highly controversial. Inflammation is likely a key mediator of vascular calcification, but immune signaling mechanisms that promote this process are minimally understood. APPROACH AND RESULTS: Here, we identify Rac2 as a major inflammatory regulator of signaling that directs plaque osteogenesis...
November 10, 2016: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/27834689/nicotine-accelerates-atherosclerosis-in-apolipoprotein-e-deficient-mice-by-activating-%C3%AE-7-nicotinic-acetylcholine-receptor-on-mast-cells
#11
Chen Wang, Han Chen, Wei Zhu, Yinchuan Xu, Ming-Fei Liu, Lian-Lian Zhu, Fan Yang, Ling Zhang, Xian-Bao Liu, Zhiwei Zhong, Jing Zhao, Jun Jiang, Meixiang Xiang, Hong Yu, Xinyang Hu, Hong Lu, Jian'an Wang
OBJECTIVE: Cigarette smoking is an independent risk factor for atherosclerosis. Nicotine, the addictive component of cigarettes, induces mast cell (MC) release and contributes to atherogenesis. The purpose of this study was to determine whether nicotine accelerates atherosclerosis through MC-mediated mechanisms and whether MC stabilizer prevents this pathological process. APPROACH AND RESULTS: Nicotine administration increased the size of atherosclerotic lesions in apolipoprotein E-deficient (Apoe(-/-)) mice fed a fat-enriched diet...
November 10, 2016: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/27822682/the-different-facets-of-dyslipidemia-and-hypertension-in-atherosclerosis
#12
REVIEW
Jessica Hurtubise, Krystie McLellan, Kevin Durr, Oluwadara Onasanya, Daniel Nwabuko, Joseph Fomusi Ndisang
Atherosclerosis is the narrowing of arteries due to the accumulation of macrophages overloaded with lipids resulting in foam cell formation, and these events occur preferentially at the branching points of arteries which are particularly susceptible to hyperlipidemic stress-induced inflammation and oxidative stress. The different stages of atherogenesis rely on oxidative stress, endothelial dysfunction, and inflammation, and hypertension or dyslipidemia can independently trigger these stages. Dyslipidemia and hypertension are pathological conditions that damage the endothelium, triggering cell proliferation, vascular remodeling, apoptosis, and increased cellular permeability with increased adhesion molecules that bind monocytes and T lymphocytes to create a vicious cocktail of pathophysiological factors...
December 2016: Current Atherosclerosis Reports
https://www.readbyqxmd.com/read/27821559/sex-steroids-block-the-initiation-of-atherosclerosis
#13
Frederick Naftolin, Holly Mehr, Ahmed Fadiel
Atherosclerosis is the main cause of death in men and women. This so-called "hardening of the arteries" results from advanced atherogenesis, the accumulation and death of subendothelial fat-laden macrophages (vascular plaque). The macrophages are attracted as the result of signals from injured vessels recruiting and activating cells to quell the injury by inflammation. Among the recruited cells are circulating monocytes that may be captured by the formation of neural cell adhesion molecule (nCAM) tethers between the monocytes and vascular endothelium; the tethers are dependent on electrostatic binding between distal segments of apposed nCAM molecules...
December 2016: Reproductive Sciences
https://www.readbyqxmd.com/read/27809851/cyclophilin-a-enhances-macrophage-differentiation-and-lipid-uptake-in-high-glucose-conditions-a-cellular-mechanism-for-accelerated-macro-vascular-disease-in-diabetes-mellitus
#14
Surya Ramachandran, Anandan Vinitha, Cheranellore Chandrasekharan Kartha
BACKGROUND: Vascular disease in diabetes is initiated by monocyte adhesion to vascular endothelium, transmigration and formation of foam cells. Increasing clinical evidence supports a role for the secretory protein, cyclophilin A in diabetic vascular disease. The means by which cyclophilin A contributes to vascular lesion development in diabetes is however largely unknown. METHODS: In this study we investigated using THP1 cells and human monocytes whether cyclophilin A under hyperglycemic conditions, functions in the inflammatory cascade as a chemoattractant and increases lipid uptake by formation of foam cells invitro...
November 3, 2016: Cardiovascular Diabetology
https://www.readbyqxmd.com/read/27789842/senescent-intimal-foam-cells-are-deleterious-at-all-stages-of-atherosclerosis
#15
Bennett G Childs, Darren J Baker, Tobias Wijshake, Cheryl A Conover, Judith Campisi, Jan M van Deursen
Advanced atherosclerotic lesions contain senescent cells, but the role of these cells in atherogenesis remains unclear. Using transgenic and pharmacological approaches to eliminate senescent cells in atherosclerosis-prone low-density lipoprotein receptor-deficient (Ldlr(-/-)) mice, we show that these cells are detrimental throughout disease pathogenesis. We find that foamy macrophages with senescence markers accumulate in the subendothelial space at the onset of atherosclerosis, where they drive pathology by increasing expression of key atherogenic and inflammatory cytokines and chemokines...
October 28, 2016: Science
https://www.readbyqxmd.com/read/27784857/developmental-endothelial-locus-1-del-1-inhibits-oxidized-low-density-lipoprotein-activity-by-direct-binding-and-its-overexpression-attenuates-atherogenesis-in-mice
#16
Akemi Kakino, Yoshiko Fujita, Atsushi Nakano, Sayaka Horiuchi, Tatsuya Sawamura
BACKGROUND: Modified low-density lipoprotein (LDL) binding to scavenger receptors has been implicated in atherosclerosis. It is hypothesized that a third molecule may affect modified LDL binding, therefore, this study focuses on the soluble endogenous protein, developmental endothelial locus-1 (Del-1), as an inhibitor of oxidized LDL (oxLDL) interactions.Methods and Results:Del-1 preferentially bound oxLDL over native LDL in a cell-free binding assay. Del-1 also inhibited DiI-labeled oxLDL uptake by scavenger receptors irrespective of the receptor type (LOX-1, SR-AI, CD36, or SR-BI) expressed in COS-7 cells, and independent of cell type (human coronary artery endothelial cells (HCAECs) or THP-1-derived macrophages)...
October 26, 2016: Circulation Journal: Official Journal of the Japanese Circulation Society
https://www.readbyqxmd.com/read/27776344/baicalein-protects-against-oxldl-caused-oxidative-stress-and-inflammation-by-modulation-of-ampk-alpha
#17
Kun-Ling Tsai, Ching-Hsia Hung, Shih-Hung Chan, Jhih-Yuan Shih, Yung-Hsin Cheng, Yi-Ju Tsai, Huei-Chen Lin, Pei-Ming Chu
Atherosclerosis is considered to be a form of chronic inflammation and a disorder of lipid metabolism. Oxidative transformations in the lipid and apolipoprotein B (Apo B) constituent of low density lipoprotein drive the initial step in atherogenesis due to macrophage scavenger receptors identify oxidized LDL (oxLDL) but non-oxidized LDL. The human vascular endothelial cells fact a critical role in vasodilation, provides a nonadhesive surface for circulation, reduces vascular smooth muscle proliferation, inflammation, thrombus formation and platelet aggregation...
October 20, 2016: Oncotarget
https://www.readbyqxmd.com/read/27762264/trem-1-links-dyslipidemia-to-inflammation-and-lipid-deposition-in-atherosclerosis
#18
Daniel Zysset, Benjamin Weber, Silvia Rihs, Jennifer Brasseit, Stefan Freigang, Carsten Riether, Yara Banz, Adelheid Cerwenka, Cedric Simillion, Pedro Marques-Vidal, Adrian F Ochsenbein, Leslie Saurer, Christoph Mueller
Triggering receptor expressed on myeloid cells-1 (TREM-1) is a potent amplifier of pro-inflammatory innate immune responses, but its significance in non-infectious diseases remains unclear. Here, we demonstrate that TREM-1 promotes cardiovascular disease by exacerbating atherosclerosis. TREM-1 is expressed in advanced human atheromas and is highly upregulated under dyslipidemic conditions on circulating and on lesion-infiltrating myeloid cells in the Apoe(-/-) mouse model. TREM-1 strongly contributes to high-fat, high-cholesterol diet (HFCD)-induced monocytosis and synergizes with HFCD serum-derived factors to promote pro-inflammatory cytokine responses and foam cell formation of human monocyte/macrophages...
October 20, 2016: Nature Communications
https://www.readbyqxmd.com/read/27757983/poly-adp-ribose-polymerase1-deficiency-increases-nitric-oxide-production-and-attenuates-aortic-atherogenesis-through-downregulation-of-arginase-ii
#19
Shu-Jian Wei, Lin Cheng, Er-Shun Liang, Qi Wang, Sheng-Nan Zhou, Hao Xu, Long-Hua Hui, Zhi-Ming Ge, Ming-Xiang Zhang
Poly (ADP-ribose) polymerase (PARP) plays an important role in endothelial dysfunction, leading to atherogenesis and vascular-related diseases. However, whether PARP regulates nitric oxide (NO), a key regulator of endothelial function, is unclear so far. We investigated whether inhibition of PARP-1, the most abundant PARP isoform, prevents atherogenesis by regulating NO production and tried to elucidate the possible mechanisms involved in this phenomenon. In apolipoprotein E-deficient (apoE(-/-) ) mice fed a high-cholesterol diet for 12 weeks, PARP-1 inhibition via treatment with 3,4-dihydro-54-(1-piperindinyl) butoxy-1(2H)-isoquinoline (DPQ) or PARP-1 gene knockoutreduced aortic atherosclerotic plaque areas (49% and 46%, respectively)...
October 18, 2016: Clinical and Experimental Pharmacology & Physiology
https://www.readbyqxmd.com/read/27755984/mirna-27b-modulates-endothelial-cell-angiogenesis-by-directly-targeting-naa15-in-atherogenesis
#20
Li Qun, Xi Wenda, Sun Weihong, Ma Jianyang, Cai Wei, Lou Fangzhou, Xu Zhenyao, Gao Pingjin
BACKGROUND AND AIMS: The CCL20/CCR6 axis has been shown to play a vital role in the pathogenesis of atherosclerosis (AS). However, the regulatory mechanism remains unclear. Here, we studied the miRNA-mediated epigenetic regulation of the CCL20/CCR6 axis in atherogenesis. METHODS: CCR6(+/+)ApoE-/- and CCR6(-/-)ApoE-/- mice were fed a high-fat diet for 24 weeks. Plaque size was evaluated via ultrasound biomicroscope and hematoxylin and eosin. Protein expression were measured by Western blotting or immunofluorescence/immunohistochemistry or ELISA, and gene mRNA levels were detected by RT-PCR...
October 8, 2016: Atherosclerosis
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