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https://www.readbyqxmd.com/read/28596373/mitochondrial-oxidative-stress-promotes-atherosclerosis-and-neutrophil-extracellular-traps-in-aged-mice
#1
Ying Wang, Wei Wang, Nan Wang, Alan R Tall, Ira Tabas
RATIONALE: Mitochondrial oxidative stress (mitoOS) has been shown to be increased in various cell types in human atherosclerosis and with aging. However, the role of cell type-specific mitoOS in atherosclerosis in the setting of advanced age and the molecular mechanisms remains to be determined in vivo. OBJECTIVE: The aim of this study was to examine the role of myeloid cell mitoOS in atherosclerosis in aged mice. APPROACH AND RESULTS: Lethally irradiated low-density lipoprotein receptor-deficient mice (Ldlr(-/-)) were reconstituted with bone marrow from either wild-type or mitochondrial catalase (mCAT) mice...
August 2017: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/28527709/boosting-inflammation-resolution-in-atherosclerosis-the-next-frontier-for-therapy
#2
REVIEW
Gabrielle Fredman, Ira Tabas
Defective inflammation resolution is the underlying cause of prevalent chronic inflammatory diseases, such as arthritis, asthma, cancer, and neurodegenerative and cardiovascular diseases. Inflammation resolution is governed by several endogenous factors, including fatty acid-derived specialized proresolving mediators and proteins, such as annexin A1. Specifically, specialized proresolving mediators comprise a family of mediators that include arachidonic acid-derived lipoxins, omega-3 fatty acid eicosapentaenoic acid-derived resolvins, docosahexaenoic acid-derived resolvins, protectins, and maresins...
June 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/28428217/microrna-33-regulates-macrophage-autophagy-in-atherosclerosis
#3
Mireille Ouimet, Hasini Ediriweera, Milessa Silva Afonso, Bhama Ramkhelawon, Ragunath Singaravelu, Xianghai Liao, Rachel C Bandler, Karishma Rahman, Edward A Fisher, Katey J Rayner, John P Pezacki, Ira Tabas, Kathryn J Moore
OBJECTIVE: Defective autophagy in macrophages leads to pathological processes that contribute to atherosclerosis, including impaired cholesterol metabolism and defective efferocytosis. Autophagy promotes the degradation of cytoplasmic components in lysosomes and plays a key role in the catabolism of stored lipids to maintain cellular homeostasis. microRNA-33 (miR-33) is a post-transcriptional regulator of genes involved in cholesterol homeostasis, yet the complete mechanisms by which miR-33 controls lipid metabolism are unknown...
June 2017: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/28068223/hepatocyte-taz-wwtr1-promotes-inflammation-and-fibrosis-in-nonalcoholic-steatohepatitis
#4
Xiaobo Wang, Ze Zheng, Jorge Matias Caviglia, Kathleen E Corey, Tina M Herfel, Bishuang Cai, Ricard Masia, Raymond T Chung, Jay H Lefkowitch, Robert F Schwabe, Ira Tabas
Nonalcoholic steatohepatitis (NASH) is a leading cause of liver disease worldwide. However, the molecular basis of how benign steatosis progresses to NASH is incompletely understood, which has limited the identification of therapeutic targets. Here we show that the transcription regulator TAZ (WWTR1) is markedly higher in hepatocytes in human and murine NASH liver than in normal or steatotic liver. Most importantly, silencing of hepatocyte TAZ in murine models of NASH prevented or reversed hepatic inflammation, hepatocyte death, and fibrosis, but not steatosis...
December 13, 2016: Cell Metabolism
https://www.readbyqxmd.com/read/28067670/mertk-receptor-cleavage-promotes-plaque-necrosis-and-defective-resolution-in-atherosclerosis
#5
Bishuang Cai, Edward B Thorp, Amanda C Doran, Brian E Sansbury, Mat J A P Daemen, Bernhard Dorweiler, Matthew Spite, Gabrielle Fredman, Ira Tabas
Atherothrombotic vascular disease is often triggered by a distinct type of atherosclerotic lesion that displays features of impaired inflammation resolution, notably a necrotic core and thinning of a protective fibrous cap that overlies the core. A key cause of plaque necrosis is defective clearance of apoptotic cells, or efferocytosis, by lesional macrophages, but the mechanisms underlying defective efferocytosis and its possible links to impaired resolution in atherosclerosis are incompletely understood. Here, we provide evidence that proteolytic cleavage of the macrophage efferocytosis receptor c-Mer tyrosine kinase (MerTK) reduces efferocytosis and promotes plaque necrosis and defective resolution...
February 1, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/27979856/2016-russell-ross-memorial-lecture-in-vascular-biology-molecular-cellular-mechanisms-in-the-progression-of-atherosclerosis
#6
Ira Tabas
Atherosclerosis is initiated by the subendothelial accumulation of apoB-lipoproteins, which initiates a sterile inflammatory response dominated by monocyte-macrophages but including all classes of innate and adaptive immune cells. These inflammatory cells, together with proliferating smooth muscle cells and extracellular matrix, promote the formation of subendothelial lesions or plaques. In the vast majority of cases, these lesions do not cause serious clinical symptoms, which is due in part to a resolution-repair response that limits tissue damage...
February 2017: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/27958361/deficiency-of-axl-in-bone-marrow-derived-cells-does-not-affect-advanced-atherosclerotic-lesion-progression
#7
Manikandan Subramanian, Jonathan D Proto, Glenn K Matsushima, Ira Tabas
AXL, a member of the TAM (Tyro3, Axl, MerTK) family of receptors, plays important roles in cell survival, clearance of dead cells (efferocytosis), and suppression of inflammation, which are processes that critically influence atherosclerosis progression. Whereas MerTK deficiency promotes defective efferocytosis, inflammation, and plaque necrosis in advanced murine atherosclerosis, the role of Axl in advanced atherosclerosis progression is not known. Towards this end, bone marrow cells from Axl(-/-) or wild-type mice were transplanted into lethally irradiated Ldlr(-/-) mice...
December 13, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27659679/an-imbalance-between-specialized-pro-resolving-lipid-mediators-and-pro-inflammatory-leukotrienes-promotes-instability-of-atherosclerotic-plaques
#8
Gabrielle Fredman, Jason Hellmann, Jonathan D Proto, George Kuriakose, Romain A Colas, Bernhard Dorweiler, E Sander Connolly, Robert Solomon, David M Jones, Eric J Heyer, Matthew Spite, Ira Tabas
Chronic unresolved inflammation plays a causal role in the development of advanced atherosclerosis, but the mechanisms that prevent resolution in atherosclerosis remain unclear. Here, we use targeted mass spectrometry to identify specialized pro-resolving lipid mediators (SPM) in histologically-defined stable and vulnerable regions of human carotid atherosclerotic plaques. The levels of SPMs, particularly resolvin D1 (RvD1), and the ratio of SPMs to pro-inflammatory leukotriene B4 (LTB4), are significantly decreased in the vulnerable regions...
September 23, 2016: Nature Communications
https://www.readbyqxmd.com/read/27437578/heart-disease-death-defying-plaque-cells
#9
COMMENT
Ira Tabas
No abstract text is available yet for this article.
August 4, 2016: Nature
https://www.readbyqxmd.com/read/27239042/hepatocyte-dach1-is-increased-in-obesity-via-nuclear-exclusion-of-hdac4-and-promotes-hepatic-insulin-resistance
#10
Lale Ozcan, Devram S Ghorpade, Ze Zheng, Jane Cristina de Souza, Ke Chen, Marc Bessler, Melissa Bagloo, Beth Schrope, Richard Pestell, Ira Tabas
Defective insulin signaling in hepatocytes is a key factor in type 2 diabetes. In obesity, activation of calcium/calmodulin-dependent protein kinase II (CaMKII) in hepatocytes suppresses ATF6, which triggers a PERK-ATF4-TRB3 pathway that disrupts insulin signaling. Elucidating how CaMKII suppresses ATF6 is therefore essential to understanding this insulin resistance pathway. We show that CaMKII phosphorylates and blocks nuclear translocation of histone deacetylase 4 (HDAC4). As a result, HDAC4-mediated SUMOylation of the corepressor DACH1 is decreased, which protects DACH1 from proteasomal degradation...
June 7, 2016: Cell Reports
https://www.readbyqxmd.com/read/27199481/mertk-cleavage-limits-proresolving-mediator-biosynthesis-and-exacerbates-tissue-inflammation
#11
Bishuang Cai, Edward B Thorp, Amanda C Doran, Manikandan Subramanian, Brian E Sansbury, Chyuan-Sheng Lin, Matthew Spite, Gabrielle Fredman, Ira Tabas
The acute inflammatory response requires a coordinated resolution program to prevent excessive inflammation, repair collateral damage, and restore tissue homeostasis, and failure of this response contributes to the pathology of numerous chronic inflammatory diseases. Resolution is mediated in part by long-chain fatty acid-derived lipid mediators called specialized proresolving mediators (SPMs). However, how SPMs are regulated during the inflammatory response, and how this process goes awry in inflammatory diseases, are poorly understood...
June 7, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27100066/targeted-interleukin-10-nanotherapeutics-developed-with-a-microfluidic-chip-enhance-resolution-of-inflammation-in-advanced-atherosclerosis
#12
Nazila Kamaly, Gabrielle Fredman, Jhalique Jane R Fojas, Manikandan Subramanian, Won Ii Choi, Katherine Zepeda, Cristian Vilos, Mikyung Yu, Suresh Gadde, Jun Wu, Jaclyn Milton, Renata Carvalho Leitao, Livia Rosa Fernandes, Moaraj Hasan, Huayi Gao, Vance Nguyen, Jordan Harris, Ira Tabas, Omid C Farokhzad
Inflammation is an essential protective biological response involving a coordinated cascade of signals between cytokines and immune signaling molecules that facilitate return to tissue homeostasis after acute injury or infection. However, inflammation is not effectively resolved in chronic inflammatory diseases such as atherosclerosis and can lead to tissue damage and exacerbation of the underlying condition. Therapeutics that dampen inflammation and enhance resolution are currently of considerable interest, in particular those that temper inflammation with minimal host collateral damage...
May 24, 2016: ACS Nano
https://www.readbyqxmd.com/read/26892964/macrophage-phenotype-and-function-in-different-stages-of-atherosclerosis
#13
REVIEW
Ira Tabas, Karin E Bornfeldt
The remarkable plasticity and plethora of biological functions performed by macrophages have enticed scientists to study these cells in relation to atherosclerosis for >50 years, and major discoveries continue to be made today. It is now understood that macrophages play important roles in all stages of atherosclerosis, from initiation of lesions and lesion expansion, to necrosis leading to rupture and the clinical manifestations of atherosclerosis, to resolution and regression of atherosclerotic lesions...
February 19, 2016: Circulation Research
https://www.readbyqxmd.com/read/26541678/how-an-artery-heals
#14
EDITORIAL
Kevin Jon Williams, Ira Tabas, Edward A Fisher
No abstract text is available yet for this article.
November 6, 2015: Circulation Research
https://www.readbyqxmd.com/read/26317499/suppression-of-adaptive-immune-cell-activation-does-not-alter-innate-immune-adipose-inflammation-or-insulin-resistance-in-obesity
#15
Manikandan Subramanian, Lale Ozcan, Devram Sampat Ghorpade, Anthony W Ferrante, Ira Tabas
Obesity-induced inflammation in visceral adipose tissue (VAT) is a major contributor to insulin resistance and type 2 diabetes. Whereas innate immune cells, notably macrophages, contribute to visceral adipose tissue (VAT) inflammation and insulin resistance, the role of adaptive immunity is less well defined. To address this critical gap, we used a model in which endogenous activation of T cells was suppressed in obese mice by blocking MyD88-mediated maturation of CD11c+ antigen-presenting cells. VAT CD11c+ cells from Cd11cCre+Myd88fl/fl vs...
2015: PloS One
https://www.readbyqxmd.com/read/26068544/treatment-of-obese-insulin-resistant-mice-with-an-allosteric-mapkapk2-3-inhibitor-lowers-blood-glucose-and-improves-insulin-sensitivity
#16
Lale Ozcan, Xiaoming Xu, Shi-Xian Deng, Devram S Ghorpade, Tiffany Thomas, Serge Cremers, Brian Hubbard, Michael H Serrano-Wu, Matthias Gaestel, Donald W Landry, Ira Tabas
The prevalence of obesity-induced type 2 diabetes (T2D) is increasing worldwide, and new treatment strategies are needed. We recently discovered that obesity activates a previously unknown pathway that promotes both excessive hepatic glucose production (HGP) and defective insulin signaling in hepatocytes, leading to exacerbation of hyperglycemia and insulin resistance in obesity. At the hub of this new pathway is a kinase cascade involving calcium/calmodulin-dependent protein kinase II (CaMKII), p38α mitogen-activated protein kinase (MAPK), and MAPKAPK2/3 (MK2/3)...
October 2015: Diabetes
https://www.readbyqxmd.com/read/25872946/c-ebp-homologous-protein-chop-in-vascular-smooth-muscle-cells-regulates-their-proliferation-in-aortic-explants-and-atherosclerotic-lesions
#17
Alex-Xianghua Zhou, Xiaobo Wang, Chyuan Sheng Lin, Jaeseok Han, Jing Yong, Marissa J Nadolski, Jan Borén, Randal J Kaufman, Ira Tabas
RATIONALE: Myeloid-derived C/EBP-homologous protein (CHOP), an effector of the endoplasmic reticulum stress-induced unfolded protein response, promotes macrophage apoptosis in advanced atherosclerosis, but the role of CHOP in vascular smooth muscle cells (VSMCs) in atherosclerosis is not known. OBJECTIVE: To investigate the role of CHOP in SM22α(+) VSMCs in atherosclerosis. METHODS AND RESULTS: Chop(fl/fl) mice were generated and crossed into the Apoe(-/-) and SM22α-CreKI(+) backgrounds...
May 22, 2015: Circulation Research
https://www.readbyqxmd.com/read/25869663/recent-insights-into-the-cellular-biology-of-atherosclerosis
#18
REVIEW
Ira Tabas, Guillermo García-Cardeña, Gary K Owens
Atherosclerosis occurs in the subendothelial space (intima) of medium-sized arteries at regions of disturbed blood flow and is triggered by an interplay between endothelial dysfunction and subendothelial lipoprotein retention. Over time, this process stimulates a nonresolving inflammatory response that can cause intimal destruction, arterial thrombosis, and end-organ ischemia. Recent advances highlight important cell biological atherogenic processes, including mechanotransduction and inflammatory processes in endothelial cells, origins and contributions of lesional macrophages, and origins and phenotypic switching of lesional smooth muscle cells...
April 13, 2015: Journal of Cell Biology
https://www.readbyqxmd.com/read/25695999/targeted-nanoparticles-containing-the-proresolving-peptide-ac2-26-protect-against-advanced-atherosclerosis-in-hypercholesterolemic-mice
#19
Gabrielle Fredman, Nazila Kamaly, Stefano Spolitu, Jaclyn Milton, Devram Ghorpade, Raymond Chiasson, George Kuriakose, Mauro Perretti, Omid Farokzhad, Ira Tabas
Chronic, nonresolving inflammation is a critical factor in the clinical progression of advanced atherosclerotic lesions. In the normal inflammatory response, resolution is mediated by several agonists, among which is the glucocorticoid-regulated protein called annexin A1. The proresolving actions of annexin A1, which are mediated through its receptor N-formyl peptide receptor 2 (FPR2/ALX), can be mimicked by an amino-terminal peptide encompassing amino acids 2-26 (Ac2-26). Collagen IV (Col IV)-targeted nanoparticles (NPs) containing Ac2-26 were evaluated for their therapeutic effect on chronic, advanced atherosclerosis in fat-fed Ldlr(-/-) mice...
February 18, 2015: Science Translational Medicine
https://www.readbyqxmd.com/read/25520521/accelerating-the-pace-of-atherosclerosis-research
#20
EDITORIAL
Alan Daugherty, Ira Tabas, Daniel J Rader
No abstract text is available yet for this article.
January 2015: Arteriosclerosis, Thrombosis, and Vascular Biology
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