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Microglia actin migration

Azizul Haque, Rachel Polcyn, Denise Matzelle, Naren L Banik
Neurodegeneration is a complex process that leads to irreversible neuronal damage and death in spinal cord injury (SCI) and various neurodegenerative diseases, which are serious, debilitating conditions. Despite exhaustive research, the cause of neuronal damage in these degenerative disorders is not completely understood. Elevation of cell surface α-enolase activates various inflammatory pathways, including the production of pro-inflammatory cytokines, chemokines, and some growth factors that are detrimental to neuronal cells...
February 18, 2018: Brain Sciences
Jun-Ichi Satoh, Yoshihiro Kino, Motoaki Yanaizu, Youhei Tosaki, Kenji Sakai, Tsuyoshi Ishida, Yuko Saito
Nasu-Hakola disease (NHD) is a rare autosomal recessive leukoencephalopathy caused by a loss-of-function mutation of either TYROBP ( DAP12 ) or TREM2 expressed in microglia. A rare variant of the TREM2 gene encoding p.Arg47His causes a 3-fold increase in the risk for late-onset Alzheimer's disease (LOAD). A recent study demonstrated that a rare coding variant p.Ser209Phe in the ABI family member 3 ( ABI3 ) gene, a regulator of actin cytoskeleton organization, confers risk of developing of LOAD, although the pattern of ABI3 expression in AD and NHD brains with relevance to microglial pathology remains to be characterized...
November 2017: Intractable & Rare Diseases Research
Muhammad Shahdaat Bin Sayeed, Qasim Alhadidi, Zahoor A Shah
Intracerebral hemorrhage (ICH) is the most severe form of stroke and is further exacerbated by the secondary injury involving inflammatory response due to the activation of microglia. This secondary injury is partly due to the toxic effects of hemin, an endogenous breakdown product of hemoglobin. Cofilin, an actin depolymerizing factor, controls actin dynamics and has been previously shown to be involved in mediating neuronal cell death in ischemic conditions and during bacterial lipopolysaccharide induced microglial activation...
December 15, 2017: Journal of Neuroimmunology
Ming-Kai Jhan, Tsung-Ting Tsai, Chia-Ling Chen, Cheng-Chieh Tsai, Yi-Lin Cheng, Yi-Chao Lee, Chiung-Yuan Ko, Yee-Shin Lin, Chih-Peng Chang, Liang-Tzung Lin, Chiou-Feng Lin
Activated microglial cells are present in dengue virus (DENV)-infected brains; however, the possible effects of DENV on microglia remain unclear. Here, we demonstrated DENV caused infection, including viral entry, RNA replication, viral protein expression, and virus release, in the murine microglial cell line BV2. DENV infection caused an increase in the formation of the multipolar phenotype in vitro and in vivo without affecting cell growth and cytotoxicity. DENV infection considerably increased cell motility and disrupting either actin filaments or clathrin retarded such effect...
March 7, 2017: Scientific Reports
Qasim Alhadidi, Zahoor A Shah
Microglial cells are activated in response to different types of injuries or stress in the CNS. Such activation is necessary to get rid of the injurious agents and restore tissue homeostasis. However, excessive activation of microglial cells is harmful and contributes to secondary injury. Pertinently, microglial cell activity was targeted in many preclinical and clinical studies but such strategy failed in clinical trials. The main reason behind the failed attempts is the complexity of the injury mechanisms which needs either a combination therapy or targeting a process that is involved in multiple pathways...
February 2018: Molecular Neurobiology
Marija Adzic, Ivana Stevanovic, Natasa Josipovic, Danijela Laketa, Irena Lavrnja, Ivana M Bjelobaba, Iva Bozic, Marija Jovanovic, Milena Milosevic, Nadezda Nedeljkovic
It is widely accepted that adenosine triphosphate (ATP) acts as a universal danger-associated molecular pattern with several known mechanisms for immune cell activation. In the central nervous system, ATP activates microglia and astrocytes and induces a neuroinflammatory response. The aim of the present study was to describe responses of isolated astrocytes to increasing concentrations of ATP (5 µM to 1 mM), which were intended to mimic graded intensity of the extracellular stimulus. The results show that ATP induces graded activation response of astrocytes in terms of the cell proliferation, stellation, shape remodeling, and underlying actin and GFAP filament rearrangement, although the changes occurred without an apparent increase in GFAP and actin protein expression...
April 2017: Journal of Neuroscience Research
Lars Bollmann, David E Koser, Rajesh Shahapure, Hélène O B Gautier, Gerhard A Holzapfel, Giuliano Scarcelli, Malte C Gather, Elke Ulbricht, Kristian Franze
Microglial cells are key players in the primary immune response of the central nervous system. They are highly active and motile cells that chemically and mechanically interact with their environment. While the impact of chemical signaling on microglia function has been studied in much detail, the current understanding of mechanical signaling is very limited. When cultured on compliant substrates, primary microglial cells adapted their spread area, morphology, and actin cytoskeleton to the stiffness of their environment...
2015: Frontiers in Cellular Neuroscience
Ria Uhlemann, Karen Gertz, Wolfgang Boehmerle, Tobias Schwarz, Christiane Nolte, Dorette Freyer, Helmut Kettenmann, Matthias Endres, Golo Kronenberg
Impaired actin filament dynamics have been associated with cellular senescence. Microglia, the resident immune cells of the brain, are emerging as a central pathophysiological player in neurodegeneration. Microglia activation, which ranges on a continuum between classical and alternative, may be of critical importance to brain disease. Using genetic and pharmacological manipulations, we studied the effects of alterations in actin dynamics on microglia effector functions. Disruption of actin dynamics did not affect transcription of genes involved in the LPS-triggered classical inflammatory response...
June 2016: Brain Structure & Function
Shijun Wang, Chun-Hsien Chu, Tessandra Stewart, Carmen Ginghina, Yifei Wang, Hui Nie, Mingri Guo, Belinda Wilson, Jau-Shyong Hong, Jing Zhang
Malformed α-Synuclein (α-syn) aggregates in neurons are released into the extracellular space, activating microglia to induce chronic neuroinflammation that further enhances neuronal damage in α-synucleinopathies, such as Parkinson's disease. The mechanisms by which α-syn aggregates activate and recruit microglia remain unclear, however. Here we show that α-syn aggregates act as chemoattractants to direct microglia toward damaged neurons. In addition, we describe a mechanism underlying this directional migration of microglia...
April 14, 2015: Proceedings of the National Academy of Sciences of the United States of America
Yun Yuan, Parakalan Rangarajan, Enci Mary Kan, Yajun Wu, Chunyun Wu, Eng-Ang Ling
BACKGROUND: Activated microglial cells release an excess of inflammatory mediators after an ischemic stroke. We reported previously that scutellarin effectively suppressed the inflammatory response induced by activated microglia in rats subjected to middle cerebral artery occlusion (MCAO); however, the mechanism via which scutellarin exerts its effects on microglial activation has not been explored. This study aimed to elucidate if scutellarin can regulate the Notch pathway that is linked to microglia activation in MCAO rat, and in lipopolysaccharide (LPS)-induced BV-2 microglia...
January 20, 2015: Journal of Neuroinflammation
Stefanie Janßen, Viktoria Gudi, Chittappen K Prajeeth, Vikramjeet Singh, Katharina Stahl, Sandra Heckers, Thomas Skripuletz, Refik Pul, Corinna Trebst, Georgios Tsiavaliaris, Martin Stangel
Microglia are resident macrophages in the central nervous system (CNS) and the primary cells that contribute to CNS inflammation in many pathological conditions. Upon any signs of brain damage, microglia become activated and undergo tremendous cellular reorganization to adopt appropriate phenotypes. They migrate to lesion areas, accumulate, phagocytose cells or cellular debris, and produce a large array of inflammatory mediators like cytokines, chemokines, reactive oxygen species, and other mediators. To cope with the extreme cellular rearrangements during activation, microglia have to be highly dynamic...
November 2014: Experimental Neurology
Anna-Karin Persson, Mark Estacion, Hyesook Ahn, Shujun Liu, Severine Stamboulian-Platel, Stephen G Waxman, Joel A Black
Microglia are motile resident immune cells of the central nervous system (CNS) that continuously explore their territories for threats to tissue homeostasis. Following CNS insult (e.g., cellular injury, infection, or ischemia), microglia respond to signals such as ATP, transform into an activated state, and migrate towards the threat. Directed migration is a complex and highly-coordinated process involving multiple intersecting cellular pathways, including signal transduction, membrane adhesion and retraction, cellular polarization, and rearrangement of cytoskeletal elements...
December 2014: Glia
Maj-Linda B Selenica, Jennifer A Alvarez, Kevin R Nash, Daniel C Lee, Chuanhai Cao, Xiaoyang Lin, Patrick Reid, Peter R Mouton, Dave Morgan, Marcia N Gordon
BACKGROUND: The chemokine (C-C motif) ligand 2 (CCL2) is a monocyte chemoattractant protein that mediates macrophage recruitment and migration during peripheral and central nervous system (CNS) inflammation. METHODS: To determine the impact of CCL2 in inflammation in vivo and to elucidate the CCL2-induced polarization of activated brain microglia, we delivered CCL2 into the brains of wild-type mice via recombinant adeno-associated virus serotype 9 (rAAV-9) driven by the chicken β-actin promoter...
2013: Journal of Neuroinflammation
Ingrid R Niesman, Nathan Zemke, Heidi N Fridolfsson, Kristofer J Haushalter, Karen Levy, Anna Grove, Rosalie Schnoor, J Cameron Finley, Piyush M Patel, David M Roth, Brian P Head, Hemal H Patel
Microglia are ramified cells that serve as central nervous system (CNS) guardians, capable of proliferation, migration, and generation of inflammatory cytokines. In non-pathological states, these cells exhibit ramified morphology with processes intermingling with neurons and astrocytes. Under pathological conditions, they acquire a rounded amoeboid morphology and proliferative and migratory capabilities. Such morphological changes require cytoskeleton rearrangements. The molecular control points for polymerization states of microtubules and actin are still under investigation...
September 2013: Molecular and Cellular Neurosciences
Younghye Moon, Joo Yeon Kim, Woon Ryoung Kim, Hyun Jung Kim, Min Jee Jang, Yoonkey Nam, Kyungjin Kim, Hyun Kim, Woong Sun
Throughout life, newly generated neuroblasts from the subventricular zone migrate toward the olfactory bulb through the rostral migratory stream. Upon brain injury, these migrating neuroblasts change their route and begin to migrate toward injured regions, which is one of the regenerative responses after brain damage. This injury-induced migration is triggered by stromal cell-derived factor 1 (SDF1) released from microglia near the damaged site; however, it is still unclear how these cells transduce SDF1 signals and change their direction...
August 2013: Stem Cells
Yisheng Zhong, Jing Wang, Xunda Luo
Integrins are a family of membrane-spanning proteins that are important receptors for cell adhesion to extracellular matrix proteins. They also provide connections between the extracellular environment and intracellular cytoskeletons and are responsible for activation of many intracellular signaling pathways. In vitro and in vivo data strongly indicate that integrin-mediated signaling events can modulate the organization of the actin cytoskeleton in trabecular meshwork (TM) cells and are associated with astrocyte migration and microglia activation of the optic nerve head in patients with primary open angle glaucoma...
2013: BioMed Research International
Ivan R Minev, Pouria Moshayedi, James W Fawcett, Stéphanie P Lacour
Soft bioengineered surfaces offer a route towards modulating the tissue responses to chronically implanted devices and may enhance their functionality. In this communication we fabricate microtopographically rich and mechanically compliant silicone surfaces for use in soft neural interfaces. We observe the interaction of primary rat microglia and astroglia with arrays of tall and short (4.7 and 0.5μm) vertically oriented polydimethylsiloxane (PDMS) micropillars and a flat PDMS surface in vitro. With the pillar size and spacing that we use (1...
June 2013: Acta Biomaterialia
Åsa Persson, Ahmed Osman, Hayde Bolouri, Carina Mallard, H Georg Kuhn
Stroke induces extensive tissue remodeling, resulting in the activation of several cell types in the brain as well as recruitment of blood-borne leucocytes. Radixin is part of a cytoskeleton linker protein family with the ability to connect transmembrane proteins to the actin cytoskeleton, promoting cell functions involving a dynamic cytoskeleton such as morphological changes, cell division and migration which are common events of different cell types after stroke. In the healthy adult brain radixin is expressed in Olig2(+) cells throughout the brain and in neural progenitor cells in the subventricular zone...
May 2013: Glia
Honghong Yao, Ming Duan, Lu Yang, Shilpa Buch
One of the hallmark features of HIV-associated neurological disease is increased activation and migration of microglia. HIV transactivator of transcription (Tat) is released from infected cells and has the ability to recruit microglia. The purpose of this study was to investigate molecular mechanisms by which recombinant Tat₁₋₇₂, but not heated-inactive Tat₁₋₇₂,induces migration of rat primary microglia. Using primary microglia in Boyden chambers, we demonstrated the role of nonmuscle myosin light-chain kinase (nmMYLK) in Tat₁₋₇₂ (14...
April 2013: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
Wanda Kwan, Ulrike Träger, Dimitrios Davalos, Austin Chou, Jill Bouchard, Ralph Andre, Aaron Miller, Andreas Weiss, Flaviano Giorgini, Christine Cheah, Thomas Möller, Nephi Stella, Katerina Akassoglou, Sarah J Tabrizi, Paul J Muchowski
In Huntington disease (HD), immune cells are activated before symptoms arise; however, it is unclear how the expression of mutant huntingtin (htt) compromises the normal functions of immune cells. Here we report that primary microglia from early postnatal HD mice were profoundly impaired in their migration to chemotactic stimuli, and expression of a mutant htt fragment in microglial cell lines was sufficient to reproduce these deficits. Microglia expressing mutant htt had a retarded response to a laser-induced brain injury in vivo...
December 2012: Journal of Clinical Investigation
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