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https://www.readbyqxmd.com/read/28091604/polyglucose-nanoparticles-with-renal-elimination-and-macrophage-avidity-facilitate-pet-imaging-in-ischaemic-heart-disease
#1
Edmund J Keliher, Yu-Xiang Ye, Gregory R Wojtkiewicz, Aaron D Aguirre, Benoit Tricot, Max L Senders, Hannah Groenen, Francois Fay, Carlos Perez-Medina, Claudia Calcagno, Giuseppe Carlucci, Thomas Reiner, Yuan Sun, Gabriel Courties, Yoshiko Iwamoto, Hye-Yeong Kim, Cuihua Wang, John W Chen, Filip K Swirski, Hsiao-Ying Wey, Jacob Hooker, Zahi A Fayad, Willem J M Mulder, Ralph Weissleder, Matthias Nahrendorf
Tissue macrophage numbers vary during health versus disease. Abundant inflammatory macrophages destruct tissues, leading to atherosclerosis, myocardial infarction and heart failure. Emerging therapeutic options create interest in monitoring macrophages in patients. Here we describe positron emission tomography (PET) imaging with (18)F-Macroflor, a modified polyglucose nanoparticle with high avidity for macrophages. Due to its small size, Macroflor is excreted renally, a prerequisite for imaging with the isotope flourine-18...
January 16, 2017: Nature Communications
https://www.readbyqxmd.com/read/28090291/macrophage-migration-inhibitory-factor-as-a-novel-biomarker-of-portopulmonary-hypertension
#2
Hilary M DuBrock, Josanna M Rodriguez-Lopez, Barbara L LeVarge, Michael P Curry, Paul A VanderLaan, Zsuzsanna K Zsengeller, Elizabeth Pernicone, Ioana R Preston, Paul B Yu, Ivana Nikolic, Dihua Xu, Ravi I Thadhani, Richard N Channick, S Ananth Karumanchi
Portopulmonary hypertension (POPH) is a poorly understood complication of liver disease associated with significant morbidity and mortality. We sought to identify novel biomarkers of POPH disease presence and severity. We performed a prospective, multicenter, case-control study involving patients with liver disease undergoing right heart catheterization. POPH cases were defined as a mean pulmonary arterial pressure (mPAP) ≥25 mmHg and pulmonary vascular resistance (PVR) >240 dynes˙s˙cm(-5). Plasma samples were collected from the systemic and pulmonary circulation, and antibody microarray was used to identify biomarkers...
December 2016: Pulmonary Circulation
https://www.readbyqxmd.com/read/28087471/il-6-promotes-m2-macrophage-polarization-by-modulating-purinergic-signaling-and-regulates-the-lethal-release-of-nitric-oxide-during-trypanosoma-cruzi-infection
#3
Liliana M Sanmarco, Nicolás E Ponce, Laura M Visconti, Natalia Eberhardt, Martin G Theumer, Ángel R Minguez, Maria P Aoki
The production of nitric oxide (NO) is a key defense mechanism against intracellular pathogens but it must be tightly controlled in order to avoid excessive detrimental oxidative stress. In this study we described a novel mechanism through which interleukin (IL)-6 mediates the regulation of NO release induced in response to Trypanosoma cruzi infection. Using a murine model of Chagas disease, we found that, in contrast to C57BL/6 wild type (WT) mice, IL-6-deficient (IL6KO) mice exhibited a dramatic increase in plasma NO levels concomitant with a significantly higher amount of circulating IL-1β and inflammatory monocytes...
January 10, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28086885/harnessing-the-early-post-injury-inflammatory-responses-for-cardiac-regeneration
#4
REVIEW
Bill Cheng, H C Chen, I W Chou, Tony W H Tang, Patrick C H Hsieh
Cardiac inflammation is considered by many as the main driving force in prolonging the pathological condition in the heart after myocardial infarction. Immediately after cardiac ischemic injury, neutrophils are the first innate immune cells recruited to the ischemic myocardium within the first 24 h. Once they have infiltrated the injured myocardium, neutrophils would then secret proteases that promote cardiac remodeling and chemokines that enhance the recruitment of monocytes from the spleen, in which the recruitment peaks at 72 h after myocardial infarction...
January 13, 2017: Journal of Biomedical Science
https://www.readbyqxmd.com/read/28065862/liposome-encapsulated-berberine-treatment-attenuates-cardiac-dysfunction-after-myocardial-infarction
#5
Iris E Allijn, Bertrand M S Czarny, Xiaoyuan Wang, Suet Yen Chong, Marek Weiler, Acarilia Eduardo da Silva, Josbert M Metselaar, Carolyn Su Ping Lam, Giorgia Pastorin, Dominique P V de Kleijn, Gert Storm, Jiong-Wei Wang, Raymond M Schiffelers
Inflammation is a known mediator of adverse ventricular remodeling after myocardial infarction (MI) that may lead to reduction of ejection fraction and subsequent heart failure. Berberine is a isoquinoline quarternary alkaloid from plants that has been associated with anti-inflammatory, anti-oxidative, and cardioprotective properties. Its poor solubility in aqueous buffers and its short half-life in the circulation upon injection, however, have been hampering the extensive usage of this natural product. We hypothesized that encapsulation of berberine into long circulating liposomes could improve its therapeutic availability and efficacy by protecting cardiac function against MI in vivo...
January 5, 2017: Journal of Controlled Release: Official Journal of the Controlled Release Society
https://www.readbyqxmd.com/read/28065861/targeting-and-modulating-infarct-macrophages-with-hemin-formulated-in-designed-lipid-based-particles-improves-cardiac-remodeling-and-function
#6
Tamar Ben-Mordechai, David Kain, Radka Holbova, Natalie Landa, La-Paz Levin, Inbar Elron-Gross, Yifat Glucksam-Galnoy, Micha S Feinberg, Rimona Margalit, Jonathan Leor
Uncontrolled activation of pro-inflammatory macrophages after myocardial infarction (MI) accelerates adverse left ventricular (LV) remodeling and dysfunction. Hemin, an iron-containing porphyrin, activates heme oxygenase-1 (HO-1), an enzyme with anti-inflammatory and cytoprotective properties. We sought to determine the effects of hemin formulated in a macrophage-targeted lipid-based carrier (denoted HA-LP) on LV remodeling and function after MI. Hemin encapsulation efficiency was ~100% at therapeutic dose levels...
January 5, 2017: Journal of Controlled Release: Official Journal of the Controlled Release Society
https://www.readbyqxmd.com/read/28062479/loss-of-macrophage-wnt-secretion-improves-remodeling-and-function-after-myocardial-infarction-in-mice
#7
Dahlia Palevski, La-Paz Levin-Kotler, David Kain, Nili Naftali-Shani, Natalie Landa, Tammy Ben-Mordechai, Tal Konfino, Radka Holbova, Natali Molotski, Rina Rosin-Arbesfeld, Richard A Lang, Jonathan Leor
BACKGROUND: Macrophages and Wnt proteins (Wnts) are independently involved in cardiac development, response to cardiac injury, and repair. However, the role of macrophage-derived Wnts in the healing and repair of myocardial infarction (MI) is unknown. We sought to determine the role of macrophage Wnts in infarct repair. METHODS AND RESULTS: We show that the Wnt pathway is activated after MI in mice. Furthermore, we demonstrate that isolated infarct macrophages express distinct Wnt pathway components and are a source of noncanonical Wnts after MI...
January 6, 2017: Journal of the American Heart Association
https://www.readbyqxmd.com/read/28057839/niacin-promotes-cardiac-healing-after-myocardial-infarction-through-activation-of-the-myeloid-prostaglandin-d2-receptor-subtype-1
#8
Deping Kong, Juanjuan Li, Yujun Shen, Guihu Liu, Shengkai Zuo, Bo Tao, Yong Ji, Ankang Lu, Michael Lazarus, Richard M Breyer, Ying Yu
Niacin is a well-established drug used to lower cholesterol and prevent cardiovascular disease (CVD) events. However, niacin also causes cutaneous flushing side effects due to release of the proresolution mediator prostaglandin (PG) D2. Recent randomized clinical trials have demonstrated that addition of niacin with laropiprant (a PGD2 receptor subtype 1 [DP1] blocker) to statin-based therapies does not significantly decrease the risk of CVD events but increases the risk of serious adverse events. Here, we tested whether, and how, niacin beneficial effects in vivo myocardial ischemia requires the activation of the PGD2/DP1 axis...
January 5, 2017: Journal of Pharmacology and Experimental Therapeutics
https://www.readbyqxmd.com/read/28045017/protective-effects-of-intercalated-disk-protein-afadin-on-chronic-pressure-overload-induced-myocardial-damage
#9
Dimitar P Zankov, Akio Shimizu, Miki Tanaka-Okamoto, Jun Miyoshi, Hisakazu Ogita
Adhesive intercellular connections at cardiomyocyte intercalated disks (IDs) support contractile force and maintain structural integrity of the heart muscle. Disturbances of the proteins at IDs deteriorate cardiac function and morphology. An adaptor protein afadin, one of the components of adherens junctions, is expressed ubiquitously including IDs. At present, the precise role of afadin in cardiac physiology or disease is unknown. To explore this, we generated conditional knockout (cKO) mice with cardiomyocyte-targeted deletion of afadin...
January 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28041873/il-33-enhances-macrophage-m2-polarization-and-protects-mice-from-cvb3-induced-viral-myocarditis
#10
Chao Wang, Chunsheng Dong, Sidong Xiong
Viral myocarditis is the inflammation caused by myocardial virus infection, and the coxsackievirus group B3 virus (CVB3) is the most common pathogen. An efficient therapeutic agent against viral myocarditis is currently unavailable. IL-33, a new member of the IL-1 cytokine superfamily, exhibits potential immunotherapeutic effect against inflammatory and autoimmune diseases. However, the functional role of IL-33 in viral myocarditis has not been investigated. To examine the therapeutic role of IL-33 in viral myocarditis, an IL-33 overexpression plasmid (pDisplay-IL-33) and IL-33 knockdown plasmid (pLL3...
December 29, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28039938/targeted-p2x7-r-shrna-delivery-attenuates-sympathetic-nerve-sprouting-and-ameliorates-cardiac-dysfunction-in-rats-with-myocardial-infarction
#11
Hongmei Gao, Jie Yin, Yugen Shi, Hesheng Hu, Xiaolu Li, Mei Xue, Wenjuan Cheng, Ye Wang, Xinran Li, Yongkang Li, Yu Wang, Suhua Yan
BACKGROUND: Inflammation-dominated sympathetic sprouting adjacent to the necrotic region following myocardial infarction (MI) has been implicated in the etiology of arrhythmias resulting in sudden cardiac death; however, the mechanisms responsible remain to be elucidated. Although P2X7 R is a key immune mediator, its role has yet to be explored. OBJECTIVE: We investigated whether P2X7 R regulates NF-κB and affects cardiac sympathetic reinnervation in rats undergoing MI...
December 31, 2016: Cardiovascular Therapeutics
https://www.readbyqxmd.com/read/28024857/calpain-inhibition-decreases-inflammatory-protein-expression-in-vessel-walls-in-a-model-of-chronic-myocardial-ischemia
#12
Brittany A Potz, Ashraf A Sabe, Nassrene Y Elmadhun, Sharif A Sabe, Benedikt J V Braun, Richard T Clements, Anny Usheva, Frank W Sellke
BACKGROUND: Emerging data suggest a link between calpain activation and the enhanced inflammatory response of the cardiovascular system. We hypothesize that calpain activation associates with altered inflammatory protein expression in correlation with the proinflammatory profile of the myocardium. Our pig hypercholesterolemic model with chronic myocardial ischemia was treated with calpain inhibitors to establish their potential to improve cardiac function. METHODS: Yorkshire swine, fed a high cholesterol diet for 4 weeks then underwent placement of an ameroid constrictor on the left circumflex artery...
December 23, 2016: Surgery
https://www.readbyqxmd.com/read/28011588/transgenic-overexpression-of-macrophage-matrix-metalloproteinase-9-exacerbates-age-related-cardiac-hypertrophy-vessel-rarefaction-inflammation-and-fibrosis
#13
Hiroe Toba, Presley L Cannon, Andriy Yabluchanskiy, Rugmani Padmanabhan Iyer, Jeanine M D'Armiento, Merry L Lindsey
Advancing age is an independent risk factor for cardiovascular disease. Matrix metalloproteinase-9 (MMP-9) is secreted by macrophages and robustly increases in the left ventricle (LV) with age. The present study investigated the effect of MMP-9 overexpression in macrophages on cardiac aging. We compared 16-21 month old C57/BL6J wild type (WT) and transgenic (TG) male and female mice (n=15-20 /group). MMP-9 overexpression amplified the hypertrophic response to aging, as evidenced by increased LV wall thickness and myocyte cross sectional areas (p<0...
December 23, 2016: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28000751/suppression-of-nlrp3-inflammasome-activation-ameliorates-chronic-kidney-disease-induced-cardiac-fibrosis-and-diastolic-dysfunction
#14
Antoinette Bugyei-Twum, Armin Abadeh, Kerri Thai, Yanling Zhang, Melissa Mitchell, Golam Kabir, Kim A Connelly
Cardiac fibrosis is a common finding in patients with chronic kidney disease. Here, we investigate the cardio-renal effects of theracurmin, a novel formulation of the polyphenolic compound curcumin, in a rat model of chronic kidney disease. Briefly, Sprague-Dawley rats were randomized to undergo sham or subtotal nephrectomy (SNx) surgery. At 3 weeks post surgery, SNx animals were further randomized to received theracurmin via once daily oral gavage or vehicle for 5 consecutive weeks. At 8 weeks post surgery, cardiac function was assessed via echocardiography and pressure volume loop analysis, followed by LV and renal tissue collection for analysis...
December 21, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27993833/nkx2-5-is-expressed-in-atherosclerotic-plaques-and-attenuates-development-of-atherosclerosis-in-apolipoprotein-e-deficient-mice
#15
Meng Du, Xiaojing Wang, Xin Tan, Xiangrao Li, Dandan Huang, Kun Huang, Liu Yang, Fengxiao Zhang, Yan Wang, Dan Huang, Kai Huang
BACKGROUND: NK2 homeobox 5 (Nkx2-5) is a cardiac homeobox transcription factor that is expressed in a broad range of cardiac sublineages. Embryos lacking Nkx2-5 are nonviable attributed to growth retardation and gross abnormalities of the heart. However, the role of Nkx2-5 in atherosclerosis remains elusive. This study aims to elucidate the specific functions of Nkx2-5 during atherogenesis and in established atherosclerotic plaques. METHODS AND RESULTS: Two types of atherosclerotic lesions were created in ApoE(-/-) mice through 2 different dietary manipulations...
December 19, 2016: Journal of the American Heart Association
https://www.readbyqxmd.com/read/27983968/cardiac-fibroblast-cytokine-profiles-induced-by-proinflammatory-or-profibrotic-stimuli-promote-monocyte-recruitment-and-modulate-macrophage-m1-m2-balance-in-vitro
#16
Claudio Humeres, Raúl Vivar, Pia Boza, Claudia Muñoz, Samir Bolivar, Renatto Anfossi, Jose Miguel Osorio, Francisco Olivares-Silva, Lorena García, Guillermo Díaz-Araya
Macrophage polarization plays an essential role in cardiac remodeling after injury, evolving from an initial accumulation of proinflammatory M1 macrophages to a greater balance of anti-inflammatory M2 macrophages. Whether cardiac fibroblasts themselves influence this process remains an intriguing question. In this work, we present evidence for a role of cardiac fibroblasts (CF) as regulators of macrophage recruitment and skewing. Adult rat CF, were treated with lipopolysaccharide (LPS) or TGF-β1, to evaluate ICAM-1 and VCAM-1 expression using Western blot and proinflammatory/profibrotic cytokine secretion using LUMINEX...
October 27, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27979856/2016-russell-ross-memorial-lecture-in-vascular-biology-molecular-cellular-mechanisms-in-the-progression-of-atherosclerosis
#17
REVIEW
Ira Tabas
Atherosclerosis is initiated by the subendothelial accumulation of apoB-containing 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...
December 15, 2016: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/27956622/%C3%AE-2-adrenergic-receptor-dependent-chemokine-receptor-2-expression-regulates-leukocyte-recruitment-to-the-heart-following-acute-injury
#18
Laurel A Grisanti, Christopher J Traynham, Ashley A Repas, Erhe Gao, Walter J Koch, Douglas G Tilley
Following cardiac injury, early immune cell responses are essential for initiating cardiac remodeling and tissue repair. We previously demonstrated the importance of β2-adrenergic receptors (β2ARs) in the regulation of immune cell localization following acute cardiac injury, with deficient leukocyte infiltration into the damaged heart. The purpose of this study was to investigate the mechanism by which immune cell-expressed β2ARs regulate leukocyte recruitment to the heart following acute cardiac injury...
December 27, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27955979/cardiac-inflammation-in-genetic-dilated-cardiomyopathy-caused-by-mybpc3-mutation
#19
Thomas L Lynch, Mohamed Ameen Ismahil, Anil G Jegga, Michael J Zilliox, Christian Troidl, Sumanth D Prabhu, Sakthivel Sadayappan
Cardiomyopathies are a leading cause of heart failure and are often caused by mutations in sarcomeric genes, resulting in contractile dysfunction and cellular damage. This may stimulate the production of a robust proinflammatory response. To determine whether myocardial inflammation is associated with cardiac dysfunction in dilated cardiomyopathy (DCM) caused by MYBPC3 mutation, we used the well-characterized cMyBP-C((t/t)) mouse model of DCM at 3months of age. Compared to wild type (WT) mice, DCM mice exhibited significantly decreased fractional shortening (36...
December 10, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27940566/glucose-regulates-the-intrinsic-inflammatory-response-of-the-heart-to-surgically-induced-hypothermic-ischemic-arrest-and-reperfusion
#20
Ahmed S Bux, Merry L Lindsey, Hernan G Vasquez, Heinrich Taegtmeyer, Romain Harmancey
We investigated the isolated working rat heart as a model to study early transcriptional remodeling induced in the setting of open heart surgery and stress hyperglycemia. Hearts of male Sprague Dawley rats were cold-arrested in Krebs-Henseleit buffer and subjected to 60 minutes normothermic reperfusion in the working mode with buffer supplemented with non-carbohydrate substrates plus glucose (25 mM) or mannitol (25 mM; osmotic control). Gene expression profiles were determined by microarray analysis and compared to that of non-perfused hearts...
December 9, 2016: Physiological Genomics
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