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Microglia process

Teng-Fei Li, Nian Gong, Yong-Xiang Wang
Aconitines, including bulleyaconitine A, probably the most bioactive and abundant alkaloids in Aconitum plant, are a group of diester C19-diterpenoid alkaloids with one acetylester group attached to C8 of the diterpenoid skeleton and one benzoylester group to C14. Hydrolysis of both groups is involved in the processing of Aconitum, a traditional Chinese medicinal approach. We recently demonstrated that bulleyaconitine A produced anti-hypersensitivity, which was mediated by stimulation of spinal microglial dynorphin A expression...
2016: Frontiers in Pharmacology
Xiao-Qian Li, Zai-Li Zhang, Wen-Fei Tan, Xi-Jia Sun, Hong Ma
Toll-like receptor 4 (TLR4) is important for the pathogenesis of inflammatory reactions and the promotion of pain processing after ischemia/reperfusion (IR) in spinal cord. Recently, C-X-C chemokine ligand 12 (CXCL12) and its receptor, C-X-C chemokine receptor 4 (CXCR4), were demonstrated to be simultaneously critical for inflammatory reactions, thereby facilitating glial activation. However, whether CXCL12/CXCR4 expression can contribute to IR-induced inflammatory pain via spinal TLR4 remained unclear. A rat model was established by 8 min of aortic arch occlusion...
2016: PloS One
Chung-Ching Chio, Mao-Tsun Lin, Ching-Ping Chang, Hung-Jung Lin
BACKGROUND: Transforming growth factor-beta 1 (TGF-β1) regulates many processes after traumatic brain injury (TBI). Both Neuro AiD(™) (MLC601) and Astragaloside (AST) attenuate microglia activation in rats with TBI. The purpose of this study was to investigate whether MLC601 or AST improves output of TBI by affecting microglial expression of TGF-β1. MATERIALS AND METHODS: Adult male Sprague-Dawley rats (120 in number) were used to investigate the contribution of TGF-β1-containing microglia in the MLC601-mediated or the AST-mediated neuroprotection in the brain trauma condition using lateral fluid-percussion injury...
October 19, 2016: European Journal of Clinical Investigation
M Asunción Barreda-Manso, Natalia Yanguas-Casás, Manuel Nieto-Sampedro, Lorenzo Romero-Ramírez
Following a central nervous system (CNS) injury, restoration of the blood-brain barrier (BBB) integrity is essential for recovering homeostasis. When this process is delayed or impeded, blood substances and cells enter the CNS parenchyma, initiating an additional inflammatory process that extends the initial injury and causes so-called secondary neuronal loss. Astrocytes and profibrotic mesenchymal cells react to the injury and migrate to the lesion site, creating a new glia limitans that restores the BBB. This process is beneficial for the resolution of the inflammation, neuronal survival and the initiation of the healing process...
October 18, 2016: Journal of Cellular Physiology
Takashi Shiromoto, Naohiko Okabe, Feng Lu, Emi Maruyama-Nakamura, Naoyuki Himi, Kazuhiko Narita, Yoshiki Yagita, Kazumi Kimura, Osamu Miyamoto
BACKGROUND AND OBJECTIVE: Endogenous neurogenesis is associated with functional recovery after stroke, but the roles it plays in such recovery processes are unknown. This study aims to clarify the roles of endogenous neurogenesis in functional recovery and motor map reorganization induced by rehabilitative therapy after stroke by using a rat model of cerebral ischemia (CI). METHODS: Ischemia was induced via photothrombosis in the caudal forelimb area of the rat cortex...
October 12, 2016: Journal of Stroke and Cerebrovascular Diseases: the Official Journal of National Stroke Association
Elisabeth Sanchez-Mejias, Victoria Navarro, Sebastian Jimenez, Maria Sanchez-Mico, Raquel Sanchez-Varo, Cristina Nuñez-Diaz, Laura Trujillo-Estrada, Jose Carlos Davila, Marisa Vizuete, Antonia Gutierrez, Javier Vitorica
The role of microglial cells in the development and progression of Alzheimer's disease (AD) has not been elucidated. Here, we demonstrated the existence of a weak microglial response in human AD hippocampus which is in contrast to the massive microglial activation observed in APP-based models. Most importantly, microglial cells displayed a prominent degenerative profile (dentate gyrus > CA3 > CA1 > parahippocampal gyrus), including fragmented and dystrophic processes with spheroids, a reduced numerical density, and a significant decrease in the area of surveillance ("microglial domain")...
October 14, 2016: Acta Neuropathologica
Manmeet K Mamik, Eugene L Asahchop, Wing F Chan, Yu Zhu, William G Branton, Brienne A McKenzie, Eric A Cohen, Christopher Power
: HIV-1 infection of the brain causes the neurodegenerative syndrome HIV-associated neurocognitive disorders (HAND), for which there is no specific treatment. Herein, we investigated the actions of insulin using ex vivo and in vivo models of HAND. Increased neuroinflammatory gene expression was observed in brains from patients with HIV/AIDS. The insulin receptor was detected on both neurons and glia, but its expression was unaffected by HIV-1 infection. Insulin treatment of HIV-infected primary human microglia suppressed supernatant HIV-1 p24 levels, reduced CXCL10 and IL-6 transcript levels, and induced peroxisome proliferator-activated receptor gamma (PPAR-γ) expression...
October 12, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
T Weber, K Namikawa, B Winter, K Müller-Brown, R Kühn, W Wurst, R W Köster
The zebrafish is a well-established model organism to study in vivo mechanisms of cell communication, differentiation and function. Existing cell ablation methods are either invasive thereby creating additional tissue damage and potential infection sites, or they rely on the cellular expression of prokaryotic enzymes and the use of antibiotic drugs as cell-death-inducing compounds. We have recently established a novel inducible genetic cell ablation system that is based on Tamoxifen-inducible Caspase8-activity, thereby exploiting mechanisms of cell death intrinsic to most cell types...
October 11, 2016: Development
L Caetano, H Pinheiro, P Patrício, A Mateus-Pinheiro, N D Alves, B Coimbra, F I Baptista, S N Henriques, C Cunha, A R Santos, S G Ferreira, V M Sardinha, J F Oliveira, A F Ambrósio, N Sousa, R A Cunha, A J Rodrigues, L Pinto, C A Gomes
Developmental risk factors, such as the exposure to stress or high levels of glucocorticoids (GCs), may contribute to the pathogenesis of anxiety disorders. The immunomodulatory role of GCs and the immunological fingerprint found in animals prenatally exposed to GCs point towards an interplay between the immune and the nervous systems in the etiology of these disorders. Microglia are immune cells of the brain, responsive to GCs and morphologically altered in stress-related disorders. These cells are regulated by adenosine A2A receptors, which are also involved in the pathophysiology of anxiety...
October 11, 2016: Molecular Psychiatry
Zhen-Nan Ye, Zong Zhuang, Ling-Yun Wu, Jing-Peng Liu, Qiang Chen, Xiang-Sheng Zhang, Meng-Liang Zhou, Zi-Huan Zhang, Wei Li, Xiao-Liang Wang, Chun-Hua Hang
Convincing evidence supports that nuclear factor kappa B (NF-κB)-meditated inflammation contributes to the adverse prognosis of aneurysmal subarachnoid hemorrhage (SAH), and pathologic neutrophil accumulation after SAH in the brain parenchyma enhances the inflammatory process. Leukotriene B4 (LTB4) is a highly potent lipid chemoattractant of neutrophils, and its biological effects are mediated primarily through the high-affinity LTB4 receptor 1 (BLT1). It is verified that NF-κB-dependent BLT1 mediates LTB4 signaling and LTB4 stimulates NF-κB-dependent inflammation via BLT1...
October 7, 2016: Brain Research
Darrell Sawmiller, Ahsan Habib, Song Li, Donna Darlington, Huayan Hou, Jun Tian, R Douglas Shytle, Adam Smith, Brian Giunta, Takashi Mori, Jun Tan
Naturally-occurring bioactive flavonoids such as diosmin significantly reduces amyloid beta (Aβ) associated pathology in Alzheimer's disease (AD) mouse models. In the present study, oral administration of diosmin reduced cerebral Aβ oligomer levels, tau-hyperphosphorylation and cognitive impairment in the 3xTg-AD mouse model through glycogen synthase kinase-3 (GSK-3) and transient receptor potential canonical 6-related mechanisms. Diosmetin, one major bioactive metabolite of diosmin, increased inhibitory GSK-3β phosphorylation, while selectively reducing γ-secretase activity, Aβ generation, tau hyperphosphorylation and pro-inflammatory activation of microglia in vitro, without altering Notch processing...
October 15, 2016: Journal of Neuroimmunology
Elodie Martin, Céline Boucher, Bertrand Fontaine, Cécile Delarasse
Alzheimer's disease (AD) is a neurodegenerative disease characterized by formation of amyloid-β (Aβ) plaques, activated microglia, and neuronal cell death leading to progressive dementia. Recent data indicate that microglia and monocyte-derived macrophages (MDM) are key players in the initiation and progression of AD, yet their respective roles remain to be clarified. As AD occurs mostly in the elderly and aging impairs myeloid functions, we addressed the inflammatory profile of microglia and MDM during aging in TgAPP/PS1 and TgAPP/PS1dE9, two transgenic AD mouse models, compared to WT littermates...
October 8, 2016: Aging Cell
Carlos Fernández-Viadero, Magdalena Jiménez-Sanz, Anzu Fernández-Pérez, Rosario Verduga Vélez, Dámaso Crespo Santiago
Brain ageing leads to a series of changes that reduce the processes of adaptation and response. These transformations can end in cognitive impairment and/or dementia. Although the cause of these changes is diverse, inflammation and oxidative stress explain some of the pathophysiological mechanisms of these anomalies of brain functioning. Neuroinflammation triggers neuronal injury through the presence of inflammatory cytokines and the activation of microglia through membrane receptors and nuclear activation factors...
June 2016: Revista Española de Geriatría y Gerontología
F Guerriero, C Sgarlata, M Francis, N Maurizi, A Faragli, S Perna, M Rondanelli, M Rollone, G Ricevuti
Due to an increasingly aging population, Alzheimer disease (AD) represents a crucial issue for the healthcare system because of its widespread prevalence and the burden of its care needs. Several hypotheses on AD pathogenesis have been proposed and current therapeutical strategies have shown limited effectiveness. In the last decade, more evidence has supported a role for neuroinflammation and immune system dysregulation in AD. It remains unclear whether astrocytes, microglia and immune cells influence disease onset, progression or both...
October 7, 2016: Aging Clinical and Experimental Research
Qiuying Zhao, Xiaohui Wu, Shuo Yan, Xiaofang Xie, Yonghua Fan, Jinqiang Zhang, Cheng Peng, Zili You
BACKGROUND: Discoveries that microglia-mediated neuroinflammation is involved in the pathological process of depression provided a new strategy for novel antidepressant therapy. Peroxisome proliferator-activated receptor γ (PPARγ) is a nuclear receptor regulating inflammation and microglial polarization and, therefore, a potential target for resolving depressive disorders. Our hypothesis was that antidepressant effects could be achieved through anti-inflammatory and neuroprotective activities by PPARγ-dependent microglia-modulating agents...
October 4, 2016: Journal of Neuroinflammation
Verónica Murta, Carina Ferrari
In recent decades, several neurodegenerative diseases have been shown to be exacerbated by systemic inflammatory processes. There is a wide range of literature that demonstrates a clear but complex relationship between the central nervous system (CNS) and the immunological system, both under naïve or pathological conditions. In diseased brains, peripheral inflammation can transform "primed" microglia into an "active" state, which can trigger stronger pathological responses. Demyelinating diseases are a group of neurodegenerative diseases characterized by inflammatory lesions associated with demyelination, which in turn induces axonal damage, neurodegeneration, and progressive loss of function...
2016: Advances in Experimental Medicine and Biology
Francisca Cornejo, Rommy von Bernhardi
As we age, a large number of physiological and molecular changes affect the normal functioning of cells, tissues, and the organism as a whole. One of the main changes is the establishment of a state of systemic inflammatory activation, which has been termed "inflamm-aging"; a mild chronic inflammation of the aging organism that reduces the ability to generate an efficient response against stressor stimuli. As any other system, the nervous system undergoes these aging-related changes; the neuroinflammatory state depends mainly on the dysregulated activation of microglia, the innate immune cells of the central nervous system (CNS) and the principal producers of reactive oxygen species...
2016: Advances in Experimental Medicine and Biology
Bernardo Castellano, Mar Bosch-Queralt, Beatriz Almolda, Nàdia Villacampa, Berta González
Microglial cells are highly dynamic cells with processes continuously moving to survey the surrounding territory. Microglia possess a broad variety of surface receptors and subtle changes in their microenvironment cause microglial cell processes to extend, retract, and interact with neuronal synaptic contacts. When the nervous system is disturbed, microglia activate, proliferate, and migrate to sites of injury in response to alert signals. Released nucleotides like ATP and UTP are among the wide range of molecules promoting microglial activation and guiding their migration and phagocytic function...
2016: Advances in Experimental Medicine and Biology
Hyunjung Baek, Minsook Ye, Geun-Hyung Kang, Chanju Lee, Gihyun Lee, Da Bin Choi, Jaehoon Jung, Hyunseong Kim, Seonhwa Lee, Jin Su Kim, Hyun-Ju Lee, Insop Shim, Jun-Ho Lee, Hyunsu Bae
Alzheimer's disease patients display neuropathological lesions, including the accumulation of amyloid-beta (Aβ) peptide and neurofibrillary tangles. Although the mechanisms causing the neurodegenerative process are largely unknown, increasing evidence highlights a critical role of immunity in the pathogenesis of Alzheimer's disease. In the present study, we investigated the role of regulatory T cells (Tregs) on Alzheimer's disease progression. First, we explored the effect of Tregs (CD4+CD25+ T cells) and Teffs (CD4+CD25- T cells) in an adoptive transfer model...
October 4, 2016: Oncotarget
J Alex Strahan, William H Walker, Taylor R Montgomery, Nancy G Forger
Minocycline, an antibiotic of the tetracycline family, inhibits microglia in many paradigms and is among the most commonly used tools for examining the role of microglia in physiological processes. Microglia may play an active role in triggering developmental neuronal cell death, although findings have been contradictory. To determine whether microglia influence developmental cell death, we treated perinatal mice with minocycline (45 mg/kg) and quantified effects on dying cells and microglial labeling using immunohistochemistry for activated caspase-3 (AC3) and ionized calcium-binding adapter molecule 1 (Iba1), respectively...
October 5, 2016: Developmental Neurobiology
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