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https://www.readbyqxmd.com/read/28480882/dysfunction-of-microglial-stat3-alleviates-depressive-behavior-via-neuron-microglia-interactions
#1
Sun-Ho Kwon, Jeong-Kyu Han, Moonseok Choi, Yong-Jin Kwon, Sung Joon Kim, Eun Hee Yi, Jae-Cheon Shin, Ik-Hyun Cho, Byung-Hak Kim, Sang Jeong Kim, Sang-Kyu Ye
Neuron-microglia interactions have a crucial role in maintaining the neuroimmune system. The balance of neuroimmune system has emerged as an important process in the pathophysiology of depression. However, how neuron-microglia interactions contribute to major depressive disorders has been poorly understood. Herein, we demonstrated that microglia-derived synaptic changes induced antidepressive-like behavior by using microglia-specific signal transducer and activator of transcription 3 (STAT3) knockout (KO) (STAT3(fl/fl);LysM-Cre(+/-)) mice...
May 8, 2017: Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology
https://www.readbyqxmd.com/read/28416596/microrna-profiling-reveals-marker-of-motor-neuron-disease-in-als-models
#2
Mariah L Hoye, Erica D Koval, Amy J Wegener, Theodore S Hyman, Chengran Yang, David R O'Brien, Rebecca L Miller, Tracy Cole, Kathleen M Schoch, Tao Shen, Tomonori Kunikata, Jean-Philippe Richard, David H Gutmann, Nicholas J Maragakis, Holly B Kordasiewicz, Joseph D Dougherty, Timothy M Miller
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder marked by the loss of motor neurons (MNs) in the brain and spinal cord, leading to fatally debilitating weakness. Because this disease predominantly affects MNs, we aimed to characterize the distinct expression profile of that cell type to elucidate underlying disease mechanisms and to identify novel targets that inform on MN health during ALS disease time course. microRNAs (miRNAs) are short, noncoding RNAs that can shape the expression profile of a cell and thus often exhibit cell-type-enriched expression...
May 31, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28379303/restoring-neuronal-progranulin-reverses-deficits-in-a-mouse-model-of-frontotemporal-dementia
#3
Andrew E Arrant, Anthony J Filiano, Daniel E Unger, Allen H Young, Erik D Roberson
Loss-of-function mutations in progranulin (GRN), a secreted glycoprotein expressed by neurons and microglia, are a common autosomal dominant cause of frontotemporal dementia, a neurodegenerative disease commonly characterized by disrupted social and emotional behaviour. GRN mutations are thought to cause frontotemporal dementia through progranulin haploinsufficiency, therefore, boosting progranulin expression from the intact allele is a rational treatment strategy. However, this approach has not been tested in an animal model of frontotemporal dementia and it is unclear if boosting progranulin could correct pre-existing deficits...
March 29, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/28298457/distinct-regulatory-effects-of-myeloid-cell-and-endothelial-cell-napdh-oxidase-2-on-blood-pressure
#4
Can Martin Sag, Moritz Schnelle, Juqian Zhang, Colin E Murdoch, Sabine Kossmann, Andrea Protti, Celio X C Santos, Greta Sawyer, Xiaohong Zhang, Heloise Mongue-Din, Daniel A Richards, Alison C Brewer, Oleksandra Prysyazhna, Lars S Maier, Philip Wenzel, Philip J Eaton, Ajay M Shah
BACKGROUND: Hypertension caused by increased renin-angiotensin system activation is associated with elevated reactive oxygen species production. Previous studies implicate NADPH oxidase (Nox) proteins as important reactive oxygen species sources during renin-angiotensin system activation, with different Nox isoforms being potentially involved. Among these, Nox2 is expressed in multiple cell types, including endothelial cells, fibroblasts, immune cells, and microglia. Blood pressure (BP) is regulated at the central nervous system, renal, and vascular levels, but the cell-specific role of Nox2 in BP regulation is unknown...
May 30, 2017: Circulation
https://www.readbyqxmd.com/read/28264694/cell-specific-deletion-of-c1qa-identifies-microglia-as-the-dominant-source-of-c1q-in-mouse-brain
#5
Maria I Fonseca, Shu-Hui Chu, Michael X Hernandez, Melody J Fang, Lila Modarresi, Pooja Selvan, Grant R MacGregor, Andrea J Tenner
BACKGROUND: The complement cascade not only provides protection from infection but can also mediate destructive inflammation. Complement is also involved in elimination of neuronal synapses which is essential for proper development, but can be detrimental during aging and disease. C1q, required for several of these complement-mediated activities, is present in the neuropil, microglia, and a subset of interneurons in the brain. METHODS: To identify the source(s) of C1q in the brain, the C1qa gene was selectively inactivated in the microglia or Thy-1(+) neurons in both wild type mice and a mouse model of Alzheimer's disease (AD), and C1q synthesis assessed by immunohistochemistry, QPCR, and western blot analysis...
March 6, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28193684/an-agonist-of-the-protective-factor-sirt1-improves-functional-recovery-and-promotes-neuronal-survival-by-attenuating-inflammation-after-spinal-cord-injury
#6
Haihong Chen, Hao Ji, Ming Zhang, Zude Liu, Lifeng Lao, Chao Deng, Jianwei Chen, Guibin Zhong
Targeting posttraumatic inflammation is crucial for improving locomotor function. SIRT1 has been shown to play a critical role in disease processes such as hepatic inflammation, rheumatoid arthritis and acute lung inflammation by regulating inflammation. However, the role of SIRT1 in spinal cord injury (SCI) is unknown. We hypothesized that SIRT1 plays an important role in improving locomotor function after SCI by regulating neuroinflammation. In this study, we investigated the effect of SIRT1 in SCI using pharmacological intervention (SRT1720) and the Mx1-Cre/loxP recombination system to knock out target genes...
February 13, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28039362/defining-the-temporal-course-of-murine-neurofibromatosis-1-optic-gliomagenesis-reveals-a-therapeutic-window-to-attenuate-retinal-dysfunction
#7
Joseph A Toonen, Yu Ma, David H Gutmann
Background: Optic gliomas arising in the neurofibromatosis type 1 (NF1) cancer predisposition syndrome cause reduced visual acuity in 30%-50% of affected children. Since human specimens are rare, genetically engineered mouse (GEM) models have been successfully employed for preclinical therapeutic discovery and validation. However, the sequence of cellular and molecular events that culminate in retinal dysfunction and vision loss has not been fully defined relevant to potential neuroprotective treatment strategies...
June 1, 2017: Neuro-oncology
https://www.readbyqxmd.com/read/27899315/injury-stimulated-sonic-hedgehog-expression-in-microglia-contributes-to-neuroinflammatory-response-in-the-mptp-model-of-parkinson-s-disease
#8
Jeong Hwi Lee, Young Cheul Chung, Eugene Bok, Hankyu Lee, Sue Hee Huh, Ji Eun Lee, Byung Kwan Jin, Hyuk Wan Ko
Parkinson's disease (PD) is a progressive neurodegenerative disorder in which dopamine (DA) neurons in the substantia nigra pars compacta (SNpc) region are selectively destroyed. Sonic hedgehog (Shh) has been well known to play a key role in a variety of processes such as embryogenesis, cell proliferation and protection, and tissue repair during inflammation. However, the evidences for the innate role of Shh in adult brain injury are presently lacking and studies have been needed to unveil the importance of Shh in the process of neurodegeneration...
January 22, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27858314/genetically-dissecting-p2rx7-expression-within-the-central-nervous-system-using-conditional-humanized-mice
#9
Michael W Metzger, Sandra M Walser, Fernando Aprile-Garcia, Nina Dedic, Alon Chen, Florian Holsboer, Eduardo Arzt, Wolfgang Wurst, Jan M Deussing
The purinergic P2X7 receptor (P2X7R) has attracted considerable interest as a potential target for various central nervous system (CNS) pathologies including affective and neurodegenerative disorders. To date, the distribution and cellular localization of the P2X7R in the brain are not fully resolved and a matter of debate mainly due to the limitations of existing tools. However, this knowledge should be a prerequisite for understanding the contribution of the P2X7R to brain disease. Here, we generated a genetic mouse model by humanizing the P2X7R in the mouse as mammalian model organism...
June 2017: Purinergic Signalling
https://www.readbyqxmd.com/read/27822501/inhibition-of-ikk%C3%AE-reduces-ethanol-consumption-in-c57bl-6j-mice
#10
Jay M Truitt, Yuri A Blednov, Jillian M Benavidez, Mendy Black, Olga Ponomareva, Jade Law, Morgan Merriman, Sami Horani, Kelly Jameson, Amy W Lasek, R Adron Harris, R Dayne Mayfield
Proinflammatory pathways in neuronal and non-neuronal cells are implicated in the acute and chronic effects of alcohol exposure in animal models and humans. The nuclear factor-κB (NF-κB) family of DNA transcription factors plays important roles in inflammatory diseases. The kinase IKKβ mediates the phosphorylation and subsequent proteasomal degradation of cytosolic protein inhibitors of NF-κB, leading to activation of NF-κB. The role of IKKβ as a potential regulator of excessive alcohol drinking had not previously been investigated...
September 2016: ENeuro
https://www.readbyqxmd.com/read/27618864/heme-oxygenase-1-mediated-neuroprotection-in-subarachnoid-hemorrhage-via-intracerebroventricular-deferoxamine
#11
Robert H LeBlanc, Ruiya Chen, Magdy H Selim, Khalid A Hanafy
BACKGROUND: Subarachnoid hemorrhage (SAH) is a devastating disease that affects over 30,000 Americans per year. Previous animal studies have explored the therapeutic effects of deferoxamine (DFX) via its iron-chelating properties after SAH, but none have assessed the necessity of microglial/macrophage heme oxygenase-1 (HO-1 or Hmox1) in DFX neuroprotection, nor has the efficacy of an intracerebroventricular (ICV) administration route been fully examined. We explored the therapeutic efficacy of systemic and ICV DFX in a SAH mouse model and its effect on microglial/macrophage HO-1...
September 13, 2016: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/27596241/the-crucial-role-of-erk2-in-demyelinating-inflammation-in-the-central-nervous-system
#12
Rentaro Okazaki, Toru Doi, Kentaro Hayakawa, Kazuhito Morioka, Osamu Imamura, Kunio Takishima, Makoto Hamanoue, Yasuhiro Sawada, Motoshi Nagao, Sakae Tanaka, Toru Ogata
BACKGROUND: Brain inflammation is a crucial component of demyelinating diseases such as multiple sclerosis. Although the initiation of inflammatory processes by the production of cytokines and chemokines by immune cells is well characterized, the processes of inflammatory aggravation of demyelinating diseases remain obscure. Here, we examined the contribution of Erk2, one of the isoforms of the extracellular signal-regulated kinase, to demyelinating inflammation. METHODS: We used the cuprizone-induced demyelinating mouse model...
2016: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/27479807/tgf%C3%AE-regulates-persistent-neuroinflammation-by-controlling-th1-polarization-and-ros-production-via-monocyte-derived-dendritic-cells
#13
Roham Parsa, Harald Lund, Ivana Tosevski, Xing-Mei Zhang, Ursula Malipiero, Jan Beckervordersandforth, Doron Merkler, Marco Prinz, Alexandra Gyllenberg, Tojo James, Andreas Warnecke, Jan Hillert, Lars Alfredsson, Ingrid Kockum, Tomas Olsson, Adriano Fontana, Tobias Suter, Robert A Harris
Intracerebral levels of Transforming Growth Factor beta (TGFβ) rise rapidly during the onset of experimental autoimmune encephalomyelitis (EAE), a mouse model of Multiple Sclerosis (MS). We addressed the role of TGFβ responsiveness in EAE by targeting the TGFβ receptor in myeloid cells, determining that Tgfbr2 was specifically targeted in monocyte-derived dendritic cells (moDCs) but not in CNS resident microglia by using bone-marrow chimeric mice. TGFβ responsiveness in moDCs was necessary for the remission phase since LysM(Cre) Tgfbr2(fl/fl) mice developed a chronic form of EAE characterized by severe demyelination and extensive infiltration of activated moDCs in the CNS...
November 2016: Glia
https://www.readbyqxmd.com/read/27468749/angiotensin-type-1a-receptors-in-the-paraventricular-nucleus-of-the-hypothalamus-control-cardiovascular-reactivity-and-anxiety-like-behavior-in-male-mice
#14
Lei Wang, Helmut Hiller, Justin A Smith, Annette D de Kloet, Eric G Krause
This study tested the hypothesis that deletion of angiotensin type 1a receptors (AT1a) from the paraventricular nucleus of hypothalamus (PVN) attenuates anxiety-like behavior, hypothalamic-pituitary-adrenal (HPA) axis activity, and cardiovascular reactivity. We used the Cre/LoxP system to generate male mice with AT1a specifically deleted from the PVN. Deletion of the AT1a from the PVN reduced anxiety-like behavior as indicated by increased time spent in the open arms of the elevated plus maze. In contrast, PVN AT1a deletion had no effect on HPA axis activation subsequent to an acute restraint challenge but did reduce hypothalamic mRNA expression for corticotropin-releasing hormone (CRH)...
September 1, 2016: Physiological Genomics
https://www.readbyqxmd.com/read/27400854/deficient-autophagy-in-microglia-impairs-synaptic-pruning-and-causes-social-behavioral-defects
#15
H-J Kim, M-H Cho, W H Shim, J K Kim, E-Y Jeon, D-H Kim, S-Y Yoon
Autism spectrum disorders (ASDs) are neurodevelopmental disorders caused by various genetic and environmental factors that result in synaptic abnormalities. ASD development is suggested to involve microglia, which have a role in synaptic refinement during development. Autophagy and related pathways are also suggested to be involved in ASDs. However, the precise roles of microglial autophagy in synapses and ASDs are unknown. Here, we show that microglial autophagy is involved in synaptic refinement and neurobehavior regulation...
July 12, 2016: Molecular Psychiatry
https://www.readbyqxmd.com/read/27342766/mtorc1-pathway-disruption-ameliorates-brain-inflammation-following-stroke-via-a-shift-in-microglia-phenotype-from-m1-type-to-m2-type
#16
Daojing Li, Chunjiong Wang, Yang Yao, Li Chen, Guiyou Liu, Rongxin Zhang, Qiang Liu, Fu-Dong Shi, Junwei Hao
Inflammatory factors secreted by microglia play an important role in focal ischemic stroke. The mammalian target of rapamycin (mTOR) pathway is a known regulator of immune responses, but the role that mTORC1 signaling plays in poststroke neuroinflammation is not clear. To explore the relationship between microglial action in the mTORC1 pathway and the impact on stroke, we administered the mTORC1 inhibitors sirolimus and everolimus to mice. Presumably, disrupting the mTORC1 pathway after focal ischemic stroke should clarify the subsequent activity of microglia...
June 24, 2016: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/27198084/cataclysmic-specificity-when-targeting-myeloid-cells
#17
Thomas Blank, Marco Prinz
The antibacterial enzyme lysozyme M (LysM) encoded by the Lyz2 gene is broadly expressed in myeloblasts, macrophages, and neutrophils, and thus has been used for a long time as a cell-specific marker for myeloid cells in mice. In order to delete loxP-site flanked genes in myeloid cells, a Cre-recombinase (Cre) expressing mouse line was created by inserting Cre-coding sequence into the translational start site of the LysM gene. In this issue of the European Journal of Immunology [2016. 46: 1529-1532], Orthgiess et al...
June 2016: European Journal of Immunology
https://www.readbyqxmd.com/read/27175482/induction-of-the-type-i-interferon-response-in-neurological-forms-of-gaucher-disease
#18
Einat B Vitner, Tamar Farfel-Becker, Natalia Santos Ferreira, Dena Leshkowitz, Piyush Sharma, Karl S Lang, Anthony H Futerman
BACKGROUND: Neuroinflammation is a key phenomenon in the pathogenesis of many neurodegenerative diseases. Understanding the mechanisms by which brain inflammation is engaged and delineating the key players in the immune response and their contribution to brain pathology is of great importance for the identification of novel therapeutic targets for these devastating diseases. Gaucher disease, the most common lysosomal storage disease, is caused by mutations in the GBA1 gene and is a significant risk factor for Parkinson's disease; in some forms of Gaucher disease, neuroinflammation is observed...
May 12, 2016: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/27145902/microglia-replenished-ohsc-a-culture-system-to-study-in-vivo-like-adult-microglia
#19
Annette Masuch, Rianne van der Pijl, Lisa Füner, Yochai Wolf, Bart Eggen, Erik Boddeke, Knut Biber
Recent data suggest that ramified microglia fulfil various tasks in the brain. However, to investigate this unique cell type cultured primary microglia are only a poor model. We here describe a method to deplete and repopulate organotypic hippocampal slice cultures (OHSC) with ramified microglia isolated from adult mouse brain creating microglia-replenished OHSC (Mrep-OHSC). Replenished microglia integrate into the tissue and ramify to a degree indistinguishable from their counterparts in the mouse brain. Moreover, wild-type slices replenished with microglia from TNFα-deficient animals provide similar results as OHSC prepared from microglia-specific TNFα-knockout mice (CX3CR1(cre) /TNFα(fl/fl) )...
August 2016: Glia
https://www.readbyqxmd.com/read/27137488/interferon-beta-signaling-in-retinal-mononuclear-phagocytes-attenuates-pathological-neovascularization
#20
Anika Lückoff, Albert Caramoy, Rebecca Scholz, Marco Prinz, Ulrich Kalinke, Thomas Langmann
Age-related macular degeneration (AMD) is a leading cause of vision loss among the elderly. AMD pathogenesis involves chronic activation of the innate immune system including complement factors and microglia/macrophage reactivity in the retina. Here, we show that lack of interferon-β signaling in the retina accelerates mononuclear phagocyte reactivity and promotes choroidal neovascularization (CNV) in the laser model of neovascular AMD Complete deletion of interferon-α/β receptor (Ifnar) using Ifnar1(-/-) mice significantly enhanced early microglia and macrophage activation in lesion areas...
2016: EMBO Molecular Medicine
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