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Cdc42 microglia

Peng Wang, Yaru Zhang, Yu Gong, Rongrong Yang, Zhuo Chen, Wenfeng Hu, Yue Wu, Minhui Gao, Xing Xu, Yibin Qin, Chao Huang
Microglia, a type of immune cell in the brain, are in a ramified status with branched processes in normal conditions. Upon pathological stimulation, microglia retract their processes and become activated. Searching methods to make the activated microglia return to ramified status would help cope with injuries induced by neuroinflammation. Here, we investigated the influence of sodium butyrate (SB), a sodium salt form of butyrate produced by fermentation of dietary fibers in the gut on microglial process. Results showed that SB induced reversible elongations of microglial process in both normal and inflammatory conditions, and these elongations were accompanied with significant changes in markers reflecting the pro-inflammatory and anti-inflammatory status of microglia...
March 2018: Neurobiology of Disease
Chao Huang, Peng Wang, Xing Xu, Yaru Zhang, Yu Gong, Wenfeng Hu, Minhui Gao, Yue Wu, Yong Ling, Xi Zhao, Yibin Qin, Rongrong Yang, Wei Zhang
Direct induction of macrophage ramification has been shown to promote an alternative (M2) polarization, suggesting that the ramified morphology may determine the function of immune cells. The ketone body metabolite β-hydroxybutyrate (BHB) elevated in conditions including fasting and low-carbohydrate ketogenic diet (KD) can reduce neuroinflammation. However, how exactly BHB impacts microglia remains unclear. We report that BHB as well as its producing stimuli fasting and KD induced obvious ramifications of murine microglia in basal and inflammatory conditions in a reversible manner, and these ramifications were accompanied with microglial profile toward M2 polarization and phagocytosis...
October 23, 2017: Glia
Kyohei Tokizane, Hiroyuki Konishi, Kumiko Makide, Hiroki Kawana, Shinichi Nakamuta, Kozo Kaibuchi, Tomohiko Ohwada, Junken Aoki, Hiroshi Kiyama
Under a quiescent state, microglia exhibit a ramified shape, rather than the amoeboid-like morphology following injury or inflammation. The manipulation of microglial morphology in vitro has not been very successful, which has impeded the progress of microglial studies. We demonstrate that lysophosphatidylserine (LysoPS), a kind of lysophospholipids, rapidly and substantially alters the morphology of primary cultured microglia to an in vivo-like ramified shape in a receptor independent manner. This mechanism is mediated by Cdc42 activity...
May 2017: Glia
C Huang, X Lu, J L Wang, L J Tong, Y Ling, B Jiang, R R Yang, W Zhang
Microglial cells are the pivotal immune cells of the central nervous system. Adult microglia cells under physiological conditions are in a ramification state with extensively branched processes. Upon disease stimulation, they retract their processes and become activated. Induction of ramification is an attracting strategy to terminate the excessive activation of microglia. Here, we investigated the influence of compound C (CC) on microglial shape. Results showed that CC reversibly induced a ramification of murine microglia in both basal and inflammatory conditions...
September 7, 2016: Neuroscience
Veronika E Neubrand, Marta Pedreño, Marta Caro, Irene Forte-Lago, Mario Delgado, Elena Gonzalez-Rey
Activated microglia play a central role in the course of neurodegenerative diseases as they secrete cytotoxic substances which lead to neuronal cell death. Understanding the mechanisms that drive activation of microglia is essential to reverse this phenotype and to protect from neurodegeneration. With some exceptions, evidence indicates that changes in cell morphology from a star shape to a round and flat shape accompany the process of activation in microglia. In this study, we investigated the effect of adipose-tissue-derived mesenchymal stem cells (ASCs), which exert important anti-inflammatory actions, in microglia morphology...
December 2014: Glia
Alejandro Villarreal, Rocío Seoane, Agustina González Torres, Gerardo Rosciszewski, Maria Florencia Angelo, Alicia Rossi, Philip A Barker, Alberto Javier Ramos
Extracellular S100B dramatically increases after brain injury. While low S100B levels are neuroprotective, micromolar S100B levels have shown in vitro to activate microglia and facilitate neuronal death. In astrocytes, S100B exposure activates nuclear factor kappa B (NF-κB) and induces pro-inflammatory mediators. On microglia and neurons S100B effects are essentially mediated by receptor for advanced glycation end products (RAGE)/NF-κB, but it is not clear if these intracellular cascades are activated by different S100B levels in astrocytes and whether increased extracellular S100B is sufficient to induce reactive gliosis...
October 2014: Journal of Neurochemistry
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
Carlos Barcia, Carmen María Ros, Valentina Annese, María Angeles Carrillo-de Sauvage, Francisco Ros-Bernal, Aurora Gómez, José Enrique Yuste, Carmen María Campuzano, Vicente de Pablos, Emiliano Fernandez-Villalba, María Trinidad Herrero
The role of microglial motility in the context of adult neurodegeneration is poorly understood. In the present work, we investigated the microanatomical details of microglia-neuron interactions in an experimental mouse model of Parkinson's disease following the intraperitoneal injection of MPTP. The specific intoxication of dopaminergic neurons induces the cellular polarization of microglia, leading to the formation of body-to-body neuron-glia contacts, called gliapses, which precede neuron elimination. Inhibiting ROCK/Cdc42-mediated microglial motility in vivo blocks the activating features of microglia, such as increased cell size and number of filopodia and diminishes their phagocyting/secreting domains, as the reduction of the Golgi apparatus and the number of microglia-neuron contacts has shown...
2012: Scientific Reports
Jun Yan, Xiao Zhou, Jing-Jing Guo, Lei Mao, Yi-Jin Wang, Jing Sun, Li-Xin Sun, Lu-Yong Zhang, Xin-Fu Zhou, Hong Liao
Nogo-66 is a 66-amino-acid-residue extracellular domain of Nogo-A, which plays a key role in inhibition neurite outgrowth of central nervous system through binding to the Nogo-66 receptor (NgR) expressed on the neuron. Recent studies have confirmed that NgR is also expressed on the surface of macrophages/microglia in multiple sclerosis, but its biological effects remain unknown. In the present study, our results demonstrated that Nogo-66 triggered microglia anti-adhesion and inhibited their migration in vitro, which was mediated by NgR...
March 2012: Journal of Neurochemistry
Guo Jun Liu, Rajini Nagarajah, Richard B Banati, Max R Bennett
Microglia in the brain possess dynamic processes that continually sample the surrounding parenchyma and respond to local insults by rapidly converging on the site of an injury. One of the chemotaxic agents responsible for this response is ATP. Here we show that the transmitter glutamate is another such chemotaxic agent. Microglia exposed to glutamate increase their cell membrane ruffling and migrate to a source of glutamate in cell culture and in spinal cord slices. This chemotaxis is meditated by alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and metabotropic glutamate receptors on the microglia...
March 2009: European Journal of Neuroscience
Roberta Bianchi, Ileana Giambanco, Rosario Donato
Extracellular S100B is known to affect astrocytic, neuronal and microglial activities, with different effects depending on its concentration. Whereas at relatively low concentrations S100B exerts trophic effects on neurons and astrocytes, at relatively high concentrations the protein causes neuronal apoptosis and activates astrocytes and microglia, thus potentially representing an endogenous factor implicated in neuroinflammation. We have reported that RAGE ligation by S100B in BV-2 microglia results in the upregulation of expression of the pro-inflammatory cyclo-oxygenase 2 (COX-2) via parallel Ras-Cdc42-Rac1-dependent activation of c-Jun NH(2) terminal protein kinase (JNK) and Ras-Rac1-dependent stimulation of NF-kappaB transcriptional activity...
April 2010: Neurobiology of Aging
Roberta Bianchi, Cecilia Adami, Ileana Giambanco, Rosario Donato
Besides exerting regulatory roles within astrocytes, the Ca2+-modulated protein of the EF-hand type S100B is released into the brain extracellular space, thereby affecting astrocytes, neurons, and microglia. However, extracellular effects of S100B vary, depending on the concentration attained and the protein being trophic to neurons up to nanomolar concentrations and causing neuronal apoptosis at micromolar concentrations. Effects of S100B on neurons are transduced by receptor for advanced glycation end products (RAGE)...
January 2007: Journal of Leukocyte Biology
Christian Hammarberg, Bertil B Fredholm, Gunnar Schulte
The adenosine A(3) receptor generally couples to the G(i) class of heterotrimeric G proteins, thereby decreasing cAMP levels and also mediating signaling via release of betagamma subunits. Here we describe the central role of phosphatidylinositol-3'-kinase (PI3K) for adenosine A(3) receptor-induced intracellular signaling to the stress-activated protein kinase p38 and the extracellular signal-regulated protein kinases ERK1/2. We used Chinese hamster ovary cells expressing the human adenosine A(3) receptor, phospho-specific antibodies and different pharmacological tools to dissect the signaling pathways involving PI3K...
January 1, 2004: Biochemical Pharmacology
K Ohsawa, Y Imai, H Kanazawa, Y Sasaki, S Kohsaka
Ionized calcium binding adaptor molecule 1, Iba1, is an EF hand calcium binding protein whose expression is restricted to macrophages/microglia. In this study, Iba1 was shown to colocalize with F-actin in membrane ruffles induced by macrophage colony-stimulating factor and in phagocytic cups formed during zymosan phagocytosis. Expression of mutant Iba1 carrying either N- or C-terminal deletions or carrying a substitution in the calcium binding domain, suppressed the membrane ruffling and the phagocytosis. These results indicate that Iba1 is a key molecule in membrane ruffling and the phagocytosis of macrophages/microglia...
September 2000: Journal of Cell Science
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