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Efferocytosis

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https://www.readbyqxmd.com/read/28067670/mertk-receptor-cleavage-promotes-plaque-necrosis-and-defective-resolution-in-atherosclerosis
#1
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...
January 9, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28060378/cd73-regulates-anti-inflammatory-signaling-between-apoptotic-cells-and-endotoxin-conditioned-tissue-macrophages
#2
Patrick S Murphy, Jing Wang, Samir P Bhagwat, Joshua C Munger, William J Janssen, Terry W Wright, Michael R Elliott
The phagocytosis of apoptotic cells (efferocytosis) shifts macrophages to an anti-inflammatory state through a set of still poorly understood soluble and cell-bound signals. Apoptosis is a common feature of inflamed tissues, and efferocytosis by tissue macrophages is thought to promote the resolution of inflammation. However, it is not clear how the exposure of tissue macrophages to inflammatory cues (e.g., PAMPs, DAMPs) in the early stages of inflammation affects immune outcomes of macrophage-apoptotic cell interactions occurring at later stages of inflammation...
January 6, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28053235/inactivation-of-rab11a-gtpase-in-macrophages-facilitates-phagocytosis-of-apoptotic-neutrophils
#3
Chunling Jiang, Zheng Liu, Rong Hu, Lulong Bo, Richard D Minshall, Asrar B Malik, Guochang Hu
The timely and efficient clearance of apoptotic neutrophils by macrophages (efferocytosis) is required for the resolution of inflammation and tissue repair, but the regulatory mechanisms remain unclear. In this study, we investigated the role of the small GTPase Ras-related protein in brain (Rab)11a in regulating efferocytosis, and on this basis the resolution of inflammatory lung injury. We observed that apoptotic neutrophil feeding induced a rapid loss of Rab11a activity in bone marrow-derived macrophages and found that depletion of Rab11a in macrophages by small interfering RNA dramatically increased the phagocytosis of apoptotic neutrophils compared with control cells...
January 4, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28011901/efferocytosis-is-impaired-in-gaucher-macrophages
#4
Elma Aflaki, Daniel K Borger, Richard J Grey, Martha Kirby, Stacie Anderson, Grisel Lopez, Ellen Sidransky
Gaucher disease, the inherited deficiency of lysosomal glucocerebrosidase, is characterized by the presence of glucosylceramide-laden macrophages resulting from impaired digestion of aged erythrocytes or apoptotic leukocytes. Studies of macrophages from patients with type 1 Gaucher disease with genotypes N370S/N370S, N370S/L444P or N370S/c.84dupG revealed that Gaucher macrophages have impaired efferocytosis resulting from reduced levels of p67phox and Rab7. The decreased Rab7 expression leads to impaired fusion of phagosomes with lysosomes...
December 23, 2016: Haematologica
https://www.readbyqxmd.com/read/28005073/rab17-mediates-differential-antigen-sorting-following-efferocytosis-and-phagocytosis
#5
Charles Yin, Yohan Kim, Dean Argintaru, Bryan Heit
Macrophages engulf and destroy pathogens (phagocytosis) and apoptotic cells (efferocytosis), and can subsequently initiate adaptive immune responses by presenting antigens derived from engulfed materials. Both phagocytosis and efferocytosis share a common degradative pathway in which the target is engulfed into a membrane-bound vesicle, respectively, termed the phagosome and efferosome, where they are degraded by sequential fusion with endosomes and lysosomes. Despite this shared maturation pathway, macrophages are immunogenic following phagocytosis but not efferocytosis, indicating that differential processing or trafficking of antigens must occur...
December 22, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/28003382/mek1-2-inhibition-promotes-macrophage-reparative-properties
#6
Matthew E Long, William E Eddy, Ke-Qin Gong, Lara L Lovelace-Macon, Ryan S McMahan, Jean Charron, W Conrad Liles, Anne M Manicone
Macrophages have important functional roles in regulating the timely promotion and resolution of inflammation. Although many of the intracellular signaling pathways involved in the proinflammatory responses of macrophages are well characterized, the components that regulate macrophage reparative properties are less well understood. We identified the MEK1/2 pathway as a key regulator of macrophage reparative properties. Pharmacological inhibition of the MEK1/2 pathway by a MEK1/2 inhibitor (MEKi) significantly increased expression of IL-4/IL-13 (M2)-responsive genes in murine bone marrow-derived and alveolar macrophages...
January 15, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28000962/hypoxia-causes-il-8-secretion-charcot-leyden-crystal-formation-and-suppression-of-corticosteroid-induced-apoptosis-in-human-eosinophils
#7
Linsey M Porter, Andrew S Cowburn, Neda Farahi, John Deighton, Stuart N Farrow, Christine A Fiddler, Jatinder K Juss, Alison M Condliffe, Edwin R Chilvers
BACKGROUND: Inflamed environments are typically hypercellular, rich in pro-inflammatory cytokines, and profoundly hypoxic. While the effects of hypoxia on neutrophil longevity and function have been widely studied, little is known about the consequences of this stimulus on eosinophils. OBJECTIVE: We sought to investigate the effects of hypoxia on several key aspects of eosinophil biology; namely secretion, survival, and their sensitivity to glucocorticosteroids (GCS), agents which normally induce eosinophil apoptosis...
December 21, 2016: Clinical and Experimental Allergy: Journal of the British Society for Allergy and Clinical Immunology
https://www.readbyqxmd.com/read/27995621/annexin-a1-promotes-timely-resolution-of-inflammation-in-murine-gout
#8
Izabela Galvão, Juliana P Vago, Livia C Barroso, Luciana P Tavares, Celso M Queiroz-Junior, Vivian V Costa, Fernanda S Carneiro, Tatiana P Ferreira, Patricia M R Silva, Flávio A Amaral, Lirlândia P Sousa, Mauro M Teixeira
Gout is a self-limited inflammatory disease caused by deposition of monosodium urate (MSU) crystals in the joints. Resolution of inflammation is an active process leading to restoration of tissue homeostasis. Here, we studied the role of Annexin A1 (AnxA1), a glucocorticoid-regulated protein that has anti-inflammatory and pro-resolving actions, in resolution of acute gouty inflammation. Injection of MSU crystals in the knee joint of mice induced inflammation that was associated with expression of AnxA1 during the resolving phase of inflammation...
December 19, 2016: European Journal of Immunology
https://www.readbyqxmd.com/read/27979856/2016-russell-ross-memorial-lecture-in-vascular-biology-molecular-cellular-mechanisms-in-the-progression-of-atherosclerosis
#9
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/27977793/elimination-of-pseudomonas-aeruginosa-through-efferocytosis-upon-binding-to-apoptotic-cells
#10
Darío Capasso, María Victoria Pepe, Jéssica Rossello, Paola Lepanto, Paula Arias, Valentina Salzman, Arlinet Kierbel
For opportunistic pathogens such as Pseudomonas aeruginosa, the mucosal barrier represents a formidable challenge. Infections develop only in patients with altered epithelial barriers. Here, we showed that P. aeruginosa interacts with a polarized epithelium, adhering almost exclusively at sites of multi-cellular junctions. In these sites, numerous bacteria attach to an extruded apoptotic cell or apoptotic body. This dead cell tropism is independent of the type of cell death, as P. aeruginosa also binds to necrotic cells...
December 2016: PLoS Pathogens
https://www.readbyqxmd.com/read/27958361/deficiency-of-axl-in-bone-marrow-derived-cells-does-not-affect-advanced-atherosclerotic-lesion-progression
#11
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/27941671/non-canonical-cell-death-induced-by-p53
#12
REVIEW
Atul Ranjan, Tomoo Iwakuma
Programmed cell death is a vital biological process for multicellular organisms to maintain cellular homeostasis, which is regulated in a complex manner. Over the past several years, apart from apoptosis, which is the principal mechanism of caspase-dependent cell death, research on non-apoptotic forms of programmed cell death has gained momentum. p53 is a well characterized tumor suppressor that controls cell proliferation and apoptosis and has also been linked to non-apoptotic, non-canonical cell death mechanisms...
December 9, 2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/27926586/hypercapnic-conditions-after-experimental-blunt-chest-trauma-increase-efferocytosis-of-alveolar-macrophages-and-reduce-local-inflammation
#13
Annette Palmer, Michael S J Eichner, Anne Rittlinger, Daniel H Seitz, Florian Gebhard, Markus S Huber-Lang, Ulrike Niesler
Blunt chest trauma induces severe local and systemic inflammatory alterations and an accumulation of apoptotic polymorphonuclear granulocytes (aPMN) in the lungs, frequently followed by bacterial infection. Alveolar macrophages (AM) represent one of the main actors for their clearance. However, little is known regarding regulatory and influencing factors of AM efferocytic and phagocytic activities. In this context, we investigated the influence of impaired gas exchange on AM activity.Male rats underwent blunt chest trauma or sham procedure and aPMN or E...
December 6, 2016: Shock
https://www.readbyqxmd.com/read/27895181/complement-protein-c1q-enhances-macrophage-foam-cell-survival-and-efferocytosis
#14
Marc C Pulanco, Jason Cosman, Minh-Minh Ho, Jessica Huynh, Karina Fing, Jacqueline Turcu, Deborah A Fraser
In the atherosclerotic lesion, macrophages ingest high levels of damaged modified low-density lipoproteins (LDLs), generating macrophage foam cells. Foam cells undergo apoptosis and, if not efficiently cleared by efferocytosis, can undergo secondary necrosis, leading to plaque instability and rupture. As a component of the innate immune complement cascade, C1q recognizes and opsonizes modified forms of LDL, such as oxidized or acetylated LDL, and promotes ingestion by macrophages in vitro. C1q was shown to be protective in an atherosclerosis model in vivo...
January 1, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/27881672/mineralocorticoid-receptor-deficiency-in-macrophages-inhibits-atherosclerosis-by-affecting-foam-cell-formation-and-efferocytosis
#15
Zhu-Xia Shen, Xiao-Qing Chen, Xue-Nan Sun, Jian-Yong Sun, Wu-Chang Zhang, Xiao-Jun Zheng, Yu-Yao Zhang, Huan-Jing Shi, Jia-Wei Zhang, Chao Li, Jun Wang, Xu Liu, Sheng-Zhong Duan
Mineralocorticoid receptor (MR) has been considered as a potential target for treating atherosclerosis. However, the cellular and molecular mechanisms are not completely understood. We aim to explore the functions and mechanisms of macrophage MR in atherosclerosis. Atherosclerosis-susceptible LDLRKO chimeric mice with bone marrow cells from floxed control (FC) mice or from myeloid MR knockout (MRKO) mice were generated and fed with high cholesterol diet. Oil red O staining showed that MRKO decreased atherosclerotic lesion area in LDLRKO mice...
November 23, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27868302/reduced-dna-methylation-of-sphingosine-1-phosphate-receptor-5-in-alveolar-macrophages-in-copd-a-potential-link-to-failed-efferocytosis
#16
Jameel Barnawi, Hubertus Jersmann, Rainer Haberberger, Sandra Hodge, Robyn Meech
BACKGROUND AND OBJECTIVE: We previously showed that alveolar macrophages from COPD patients are defective in their ability to phagocytose apoptotic cells ('efferocytosis') and that this defect is potentially linked to the sphingosine-1 phosphate (S1P) system, in particular the sphingosine-1 phosphate receptor 5 (S1PR5). In alveolar macrophages from COPD patients, S1PR5 mRNA expression levels increased and were correlated with both lung function and efferocytosis. However, it us unknown whether these changes are under epigenetic control via DNA methylation or whether DNA methylation directly modulates macrophage function...
February 2017: Respirology: Official Journal of the Asian Pacific Society of Respirology
https://www.readbyqxmd.com/read/27853832/old-drugs-with-new-skills-fenoprofen-as-an-allosteric-enhancer-at-melanocortin-receptor-3
#17
Trinidad Montero-Melendez, Rachel A E Forfar, Jennifer M Cook, Jeffrey C Jerman, Debra L Taylor, Mauro Perretti
The efficiency of drug research and development has paradoxically declined over the last decades despite major scientific and technological advances, promoting new cost-effective strategies such as drug repositioning by systematic screening for new actions of known drugs. Here, we performed a screening for positive allosteric modulators (PAMs) at melanocortin (MC) receptors. The non-steroidal anti-inflammatory drug fenoprofen, but not the similar compound ibuprofen, presented PAM activity at MC3, MC4, and MC5 receptors...
November 16, 2016: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/27834816/targeting-the-tam-receptors-in-leukemia
#18
REVIEW
Madeline G Huey, Katherine A Minson, H Shelton Earp, Deborah DeRyckere, Douglas K Graham
Targeted inhibition of members of the TAM (TYRO-3, AXL, MERTK) family of receptor tyrosine kinases has recently been investigated as a novel strategy for treatment of hematologic malignancies. The physiologic functions of the TAM receptors in innate immune control, natural killer (NK) cell differentiation, efferocytosis, clearance of apoptotic debris, and hemostasis have previously been described and more recent data implicate TAM kinases as important regulators of erythropoiesis and megakaryopoiesis. The TAM receptors are aberrantly or ectopically expressed in many hematologic malignancies including acute myeloid leukemia, B- and T-cell acute lymphoblastic leukemia, chronic lymphocytic leukemia, and multiple myeloma...
November 8, 2016: Cancers
https://www.readbyqxmd.com/read/27827458/microrna-126-overexpression-rescues-diabetes-induced-impairment-in-efferocytosis-of-apoptotic-cardiomyocytes
#19
Sahana Suresh Babu, Rajarajan A Thandavarayan, Darukeshwara Joladarashi, Prince Jeyabal, Shashirekha Krishnamurthy, Arvind Bhimaraj, Keith A Youker, Prasanna Krishnamurthy
Efferocytosis, a process of clearance of apoptotic cells by phagocytes, is essential for successful resolution of inflammation and maintenance of tissue homeostasis. Diabetes compromises the function of macrophages leading to adverse inflammatory response during wound healing, myocardial injury, atherosclerosis and autoimmune disorders. However, the effect of diabetes on macrophage-mediated efferocytosis of apoptotic cardiomyocytes (ACM) and the molecular mechanisms involved are not understood so far. In the present study we found that invitro efferocytosis of ACM was impaired in macrophages from db/db (diabetic) mice...
November 9, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27815871/quantitative-efferocytosis-assays
#20
Amanda L Evans, Jack W D Blackburn, Charles Yin, Bryan Heit
Efferocytosis, the phagocytic removal of apoptotic cells, is a dynamic process requiring recruitment of numerous regulatory proteins to forming efferosomes in a tightly regulated manner. Herein we describe microscopy-based methods for the enumeration of efferocytic events and characterization of the spatiotemporal dynamics of signaling molecule recruitment to efferosomes, using genetically encoded probes and immunofluorescent labeling. While these methods are illustrated using macrophages, they are applicable to any efferocytic cell type...
2017: Methods in Molecular Biology
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