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https://www.readbyqxmd.com/read/28210215/tryptanthrin-suppresses-the-activation-of-the-lps-treated-bv2-microglial-cell-line-via-nrf2-ho-1-antioxidant-signaling
#1
Young-Won Kwon, So Yeong Cheon, Sung Yun Park, Juhyun Song, Ju-Hee Lee
Microglia are the resident macrophages in the central nervous system (CNS) and play essential roles in neuronal homeostasis and neuroinflammatory pathologies. Recently, microglia have been shown to contribute decisively to neuropathologic processes after ischemic stroke. Furthermore, natural compounds have been reported to attenuate inflammation and pathologies associated with neuroinflammation. Tryptanthrin (indolo[2,1-b]quinazoline-6,12-dione) is a phytoalkaloid with known anti-inflammatory effects in cells...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28171699/c-reactive-protein-in-the-detection-of-post-stroke-infections-systematic-review-and-individual-participant-data-analysis
#2
Alejandro Bustamante, Andrea Vilar-Bergua, Sophie Guettier, Josep Sánchez-Poblet, Teresa García-Berrocoso, Dolors Giralt, Felix Fluri, Raffi Topakian, Hans Worthmann, Andreas Hug, Tihamer Molnar, Ulrike Waje-Andreassen, Mira Katan, Craig J Smith, Joan Montaner
We conducted a systematic review and individual participant data meta-analysis to explore the role of C-reactive protein (CRP) in early detection or prediction of post-stroke infections. CRP, an acute-phase reactant binds to the phosphocholine expressed on the surface of dead or dying cells and some bacteria, thereby activating complement and promoting phagocytosis by macrophages. We searched PubMed up to May-2015 for studies measuring CRP in stroke and evaluating post-stroke infections. Individual participants' data were merged into a single database...
February 7, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28168325/macrophages-in-vascular-inflammation-and-atherosclerosis
#3
REVIEW
Clement Cochain, Alma Zernecke
Atherosclerosis is characterized by lipid accumulation and chronic inflammation of the arterial wall, and its main complications-myocardial infarction and ischemic stroke-together constitute the first cause of death worldwide. Accumulation of lipid-laden macrophage foam cells in the intima of inflamed arteries has long been recognized as a hallmark of atherosclerosis. However, in recent years, an unexpected complexity in the mechanisms of macrophage accumulation in lesions, in the protective and pathogenic functions performed by macrophages and how they are regulated has been uncovered...
February 6, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/28165057/a-novel-indication-of-platonin-a-therapeutic-immunomodulating-medicine-on-neuroprotection-against-ischemic-stroke-in-mice
#4
Joen-Rong Sheu, Zhih-Cherng Chen, Thanasekaran Jayakumar, Duen-Suey Chou, Ting-Lin Yen, Hsing-Ni Lee, Szu-Han Pan, Chih-Hsuan Hsia, Chih-Hao Yang, Cheng-Ying Hsieh
Thrombosis and stroke are major causes of disability and death worldwide. However, the regular antithrombotic drugs may have unsatisfactory results and side effects. Platonin, a cyanine photosensitizing dye, has been used to treat trauma, ulcers and some acute inflammation. Here, we explored the neuroprotective effects of platonin against middle cerebral artery occlusion (MCAO)-induced ischemic stroke in mice. Platonin(200 μg/kg) substantially reduced cerebral infarct volume, brain edema, neuronal cell death and neurological deficit scores, and improved the MCAO-reduced locomotor activity and rotarod performance...
February 6, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28155572/exploring-the-role-of-microglia-in-cortical-spreading-depression-in-neurological-disease
#5
Mamoru Shibata, Norihiro Suzuki
Microglia play a pivotal role in innate immunity in the brain. During development, they mature from myeloerythroid progenitor cells in the yolk sac and colonize the brain to establish a resident population of tissue macrophages. In the postnatal brain, they exert phagocytosis and induce inflammatory response against invading pathogens. Microglia also act as guardians of brain homeostasis by surveying the microenvironment using motile processes. Cortical spreading depression (CSD) is a slowly propagating (2-5 mm/min) wave of rapid, near-complete depolarization of neurons and astrocytes followed by a period of electrical suppression of a distinct population of cortical neurons...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/28137866/endothelium-targeted-overexpression-of-heat-shock-protein-27-ameliorates-blood-brain-barrier-disruption-after-ischemic-brain-injury
#6
Yejie Shi, Xiaoyan Jiang, Lili Zhang, Hongjian Pu, Xiaoming Hu, Wenting Zhang, Wei Cai, Yanqin Gao, Rehana K Leak, Richard F Keep, Michael V L Bennett, Jun Chen
The damage borne by the endothelial cells (ECs) forming the blood-brain barrier (BBB) during ischemic stroke and other neurological conditions disrupts the structure and function of the neurovascular unit and contributes to poor patient outcomes. We recently reported that structural aberrations in brain microvascular ECs-namely, uncontrolled actin polymerization and subsequent disassembly of junctional proteins, are a possible cause of the early onset BBB breach that arises within 30-60 min of reperfusion after transient focal ischemia...
February 14, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28115719/immunoinhibitory-checkpoint-deficiency-in-medium-and-large-vessel-vasculitis
#7
Hui Zhang, Ryu Watanabe, Gerald J Berry, Augusto Vaglio, Yaping Joyce Liao, Kenneth J Warrington, Jörg J Goronzy, Cornelia M Weyand
Giant cell arteritis (GCA) causes autoimmune inflammation of the aorta and its large branches, resulting in aortic arch syndrome, blindness, and stroke. CD4(+) T cells and macrophages form organized granulomatous lesions in the walls of affected arteries, destroy the tunica media, and induce ischemic organ damage through rapid intimal hyperplasia and luminal occlusion. Pathogenic mechanisms remain insufficiently understood; specifically, it is unknown whether the unopposed activation of the immune system is because of deficiency of immunoinhibitory checkpoints...
February 7, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28112757/reversal-of-maladaptive-fibrosis-and-compromised-ventricular-function-in-the-pressure-overloaded-heart-by-a-caveolin-1-surrogate-peptide
#8
Dorea Pleasant-Jenkins, Charles Reese, Panneerselvem Chinnakkannu, Harinath Kasiganesan, Elena Tourkina, Stanley Hoffman, Dhandapani Kuppuswamy
Chronic ventricular pressure overload (PO) results in congestive heart failure (CHF) in which myocardial fibrosis develops in concert with ventricular dysfunction. Caveolin-1 is important in fibrosis in various tissues due to its decreased expression in fibroblasts and monocytes. The profibrotic effects of low caveolin-1 can be blocked with the caveolin-1 scaffolding domain peptide (CSD, a caveolin-1 surrogate) using both mouse models and human cells. We have studied the beneficial effects of CSD on mice in which PO was induced by trans-aortic constriction (TAC)...
January 23, 2017: Laboratory Investigation; a Journal of Technical Methods and Pathology
https://www.readbyqxmd.com/read/28109273/blocking-of-platelet-glycoprotein-receptor-ib-reduces-thrombo-inflammation-in-mice-with-acute-ischemic-stroke
#9
Michael K Schuhmann, Josua Guthmann, Guido Stoll, Bernhard Nieswandt, Peter Kraft, Christoph Kleinschnitz
BACKGROUND: Ischemic stroke causes a strong inflammatory response that includes T cells, monocytes/macrophages, and neutrophils. Interaction of these immune cells with platelets and endothelial cells facilitates microvascular dysfunction and leads to secondary infarct growth. We recently showed that blocking of platelet glycoprotein (GP) receptor Ib improves stroke outcome without increasing the risk of intracerebral hemorrhage. Until now, it has been unclear whether GPIb only mediates thrombus formation or also contributes to the pathophysiology of local inflammation...
January 21, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28101763/mir-126-affects-brain-heart-interaction-after-cerebral-ischemic-stroke
#10
Jieli Chen, Chengcheng Cui, Xiaoping Yang, Jiang Xu, Poornima Venkat, Alex Zacharek, Peng Yu, Michael Chopp
Cardiovascular diseases are approximately three times higher in patients with neurological deficits than in patients without neurological deficits. MicroRNA-126 (MiR-126) facilitates vascular remodeling and decreases fibrosis and is emerging as an important factor in the pathogenesis of cardiovascular diseases and cerebral stroke. In this study, we tested the hypothesis that decreased miR-126 after ischemic stroke may play an important role in regulating cardiac function. Wild-type (WT), specific conditional-knockout endothelial cell miR-126 (miR-126(EC-/-)), and miR-126 knockout control (miR-126(fl/fl)) mice were subjected to distal middle cerebral artery occlusion (dMCAo) (n = 10/group)...
January 19, 2017: Translational Stroke Research
https://www.readbyqxmd.com/read/28086932/spontaneous-ischaemic-stroke-lesions-in-a-dog-brain-neuropathological-characterisation-and-comparison-to-human-ischaemic-stroke
#11
COMPARATIVE STUDY
Barbara Blicher Thomsen, Hanne Gredal, Martin Wirenfeldt, Bjarne Winther Kristensen, Bettina Hjelm Clausen, Anders Elm Larsen, Bente Finsen, Mette Berendt, Kate Lykke Lambertsen
BACKGROUND: Dogs develop spontaneous ischaemic stroke with a clinical picture closely resembling human ischaemic stroke patients. Animal stroke models have been developed, but it has proved difficult to translate results obtained from such models into successful therapeutic strategies in human stroke patients. In order to face this apparent translational gap within stroke research, dogs with ischaemic stroke constitute an opportunity to study the neuropathology of ischaemic stroke in an animal species...
January 13, 2017: Acta Veterinaria Scandinavica
https://www.readbyqxmd.com/read/28061814/cx3c-chemokine-receptor-1-deficiency-modulates-microglia-morphology-but-does-not-affect-lesion-size-and-short-term-deficits-after-experimental-stroke
#12
Gerlinde van der Maten, Vivien Henck, Tadeusz Wieloch, Karsten Ruscher
BACKGROUND: The fractalkine/CX3C chemokine receptor 1 (CX3CR1) pathway has been identified to play an essential role in the chemotaxis of microglia, leukocyte trafficking and microglia/macrophage recruitment. It has also been shown to be important in the regulation of the inflammatory response in the early phase after experimental stroke. The present study was performed to investigate if CX3CR1 deficiency affects microglia during the first 14 days with consequences for tissue damage after experimental stroke...
January 6, 2017: BMC Neuroscience
https://www.readbyqxmd.com/read/28052874/inhibition-of-hdac6-protects-against-rhabdomyolysis-induced-acute-kidney-injury
#13
Shi Yingfeng, Xu Liuqing, Tang Jinhua, Fang Lu, Ma Shuchen, Ma Xiaoyan, Nie Jing, Pi Xiaoling, Qiu Andong, Zhuang Shougang, Liu Na
Histone deacetylase 6 (HDAC6) inhibition has been reported to protect against ischemic stroke and prolong survival after sepsis in animal models. However, it remains unknown whether HDAC6 inhibition offers a renoprotective effect after acute kidney injury (AKI). In this study, we examined the therapeutic effect of tubastatin A (TA), a highly selective inhibitor of HDAC6, on AKI in a murine model of glycerol (GL) injection-induced rhabdomyolysis. Following GL injection, the mice developed severe acute tubular injury as indicated by renal dysfunction, expression of neutrophil gelatinase-associated lipocalin (NGAL), an injury marker of renal tubules and increase of TUNEL positive tubular cells...
January 4, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28049200/a-mouse-model-of-post-stroke-pneumonia-induced-by-intra-tracheal-inoculation-with-streptococcus-pneumoniae
#14
Eva Mracsko, Sabine Stegemann-Koniszewski, Shin-Young Na, Alexander Dalpke, Dunja Bruder, Felix Lasitschka, Roland Veltkamp
BACKGROUND: Stroke-induced immunodeficiency increases the risk of infectious complications, which adversely affects neurological outcome. Among those, pneumonia affects as many as one third of stroke patients and is the main contributor to mortality in the post-acute phase of stroke. Experimental findings on post-stroke susceptibility to spontaneous pneumonia in mice are contradictory. Here, we established a mouse model inducing standardized bacterial pneumonia and characterized the impaired pulmonary cellular and humoral immune responses after experimental stroke...
January 4, 2017: Cerebrovascular Diseases
https://www.readbyqxmd.com/read/28011882/mycophenolate-mofetil-prevents-cerebrovascular-injury-in-stroke-prone-spontaneously-hypertensive-rats
#15
Isha Dhande, Yaming Zhu, Michael C Braun, M John Hicks, Scott E Wenderfer, Peter A Doris
BACKGROUND AND PURPOSE: Stroke-prone spontaneously hypertensive rats (SHR-A3) develop strokes and progressive kidney disease as a result of naturally occurring genetic variations. We recently identified genetic variants in immune signaling pathways that contribute to end-organ injury. The present study was designed to test the hypothesis that a dysregulated immune response promotes stroke susceptibility. METHODS: 20-week old male SHR-A3 rats were salt loaded and treated with the immunosuppressant mycophenolate mofetil (MMF, 25 mg/kg/day, p...
December 23, 2016: Physiological Genomics
https://www.readbyqxmd.com/read/27988839/dr%C3%AE-1-mog-35-55-reduces-permanent-ischemic-brain-injury
#16
Jianyi Wang, Qing Ye, Jing Xu, Gil Benedek, Haiyue Zhang, Yuanyuan Yang, Huan Liu, Roberto Meza-Romero, Arthur A Vandenbark, Halina Offner, Yanqin Gao
Stroke induces a catastrophic immune response that involves the global activation of peripheral leukocytes, especially T cells. The human leukocyte antigen-DRα1 domain linked to MOG-35-55 peptide (DRα1-MOG-35-55) is a partial major histocompatibility complex (MHC) class II construct which can inhibit neuroantigen-specific T cells and block binding of the cytokine/chemokine macrophage migration inhibitory factor (MIF) to its CD74 receptor on monocytes and macrophages. Here, we evaluated the therapeutic effect of DRα1-MOG-35-55 in a mouse model of permanent distal middle cerebral artery occlusion (dMCAO)...
December 17, 2016: Translational Stroke Research
https://www.readbyqxmd.com/read/27988459/suppression-of-lps-induced-nf-%C3%AE%C2%BAb-activity-in-macrophages-by-the-synthetic-aurone-z-2-5-hydroxymethyl-furan-2-yl-methylene-benzofuran-3-2h-one
#17
Hyo S Park, David E Nelson, Zachary E Taylor, James B Hayes, Kirsten D Cunningham, Brock A Arivett, Rajarshi Ghosh, Larissa C Wolf, Kimberley M Taylor, Mary B Farone, Scott T Handy, Anthony L Farone
Suppressing cytokine responses has frequently been shown to have promising therapeutic effects for many chronic inflammatory and autoimmune diseases. However, the severe side effects associated with the long-term use of current treatments, such as allergic reactions and increased risk of stroke, have focused attention towards the targeting of intracellular signaling mechanisms, such as NF-κB, that regulate inflammation. We synthesized a series of non-natural aurone derivatives and investigated their ability to suppress pro-inflammatory signaling in human monocyte (THP-1) and murine macrophage-like (RAW 267...
February 2017: International Immunopharmacology
https://www.readbyqxmd.com/read/27987324/tudca-an-agonist-of-the-bile-acid-receptor-gpbar1-tgr5-with-anti-inflammatory-effects-in-microglial-cells
#18
Natalia Yanguas-Casás, M Asunción Barreda-Manso, Manuel Nieto-Sampedro, Lorenzo Romero-Ramírez
Bile acids are steroid acids found in the bile of mammals. The bile acid conjugate tauroursodeoxycholic acid (TUDCA) is neuroprotective in different animal models of stroke and neurological diseases. We have previously shown that TUDCA has anti-inflammatory effects on glial cell cultures and in a mouse model of acute neuroinflammation. We show now that microglial cells (central nervous system resident macrophages) express the G protein-coupled bile acid receptor 1/ Takeda G protein-coupled receptor 5 (GPBAR1/TGR5) in vivo and in vitro...
December 17, 2016: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/27979856/2016-russell-ross-memorial-lecture-in-vascular-biology-molecular-cellular-mechanisms-in-the-progression-of-atherosclerosis
#19
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/27932558/petct-imaging-of-unstable-carotid-plaque-with-ga-68-labelled-somatostatin-receptor-ligand
#20
Ming Young Simon Wan, Raymond Endozo, Sofia Michopoulou, Robert Shortman, Manuel Rodriguez-Justo, Leon Menezes, Syed Yusuf, Toby Richards, Damian Wild, Beatrice Waser, Jean Claude Reubi, Ashley Groves
BACKGROUND: Ga68 labelled somatostatin receptor ligand PET imaging has recently been shown in preclinical and early human studies to have a potential role in the evaluation of vulnerable arterial plaques. We prospectively evaluated carotid plaque Ga68-DOTATATE uptake in patients with recent carotid events, assessed inter- and intra- observer variability of such measurements, and explored the mechanism of any plaque DOTATATE activity with immunohistochemistry in resected specimens. MATERIALS & METHODS: 20 consecutively consenting patients with recent symptomatic carotid events (transient ischaemic attack [TIA], stroke or amaurosis fugax), due for carotid endarterectomy were prospectively recruited...
December 8, 2016: Journal of Nuclear Medicine: Official Publication, Society of Nuclear Medicine
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