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https://www.readbyqxmd.com/read/27699246/mutyh-promotes-oxidative-microglial-activation-and-inherited-retinal-degeneration
#1
Shunji Nakatake, Yusuke Murakami, Yasuhiro Ikeda, Noriko Morioka, Takashi Tachibana, Kohta Fujiwara, Noriko Yoshida, Shoji Notomi, Toshio Hisatomi, Shigeo Yoshida, Tatsuro Ishibashi, Yusaku Nakabeppu, Koh-Hei Sonoda
Oxidative stress is implicated in various neurodegenerative disorders, including retinitis pigmentosa (RP), an inherited disease that causes blindness. The biological and cellular mechanisms by which oxidative stress mediates neuronal cell death are largely unknown. In a mouse model of RP (rd10 mice), we show that oxidative DNA damage activates microglia through MutY homolog-mediated (MUYTH-mediated) base excision repair (BER), thereby exacerbating retinal inflammation and degeneration. In the early stage of retinal degeneration, oxidative DNA damage accumulated in the microglia and caused single-strand breaks (SSBs) and poly(ADP-ribose) polymerase activation...
September 22, 2016: JCI Insight
https://www.readbyqxmd.com/read/27663279/poly-adp-ribose-polymerase-is-not-involved-in-the-neuroprotection-exerted-by-azithromycin-against-ischemic-stroke-in-mice
#2
Francesco Petrelli, Mirko Muzzi, Alberto Chiarugi, Giacinto Bagetta, Diana Amantea
Repurposing azithromycin has recently emerged as a promising strategy for the acute treatment of ischemic stroke. The mechanism of neuroprotection depends on the ability of this macrolide to promote polarization of microglia/macrophages towards beneficial M2 phenotypes. The immunomodulatory and anti-inflammatory effects of azithromycin, well documented in chronic inflammatory airway diseases, have been ascribed to the inhibition of the transcription factors nuclear factor (NF)-κB and activator protein (AP)-1...
September 20, 2016: European Journal of Pharmacology
https://www.readbyqxmd.com/read/27658543/platelet-cd40l-induces-activation-of-astrocytes-and-microglia-in-hypertension
#3
Shahnawaz Ali Bhat, Ruby Goel, Rakesh Shukla, Kashif Hanif
Studies have demonstrated separately that hypertension is associated with platelet activation in the periphery (resulting in accumulation and localized inflammatory response) and glial activation in the brain. We investigated the contribution of platelets in brain inflammation, particularly glial activation in vitro and in a rat model of hypertension. We found that HTN increased the expression of adhesion molecules like JAM-1, ICAM-1, and VCAM-1 on brain endothelium and resulted in the deposition of platelets in the brain...
September 19, 2016: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/27444121/microglial-activation-induced-by-the-alarmin-s100b-is-regulated-by-poly-adp-ribose-polymerase-1
#4
Jianguo Xu, Handong Wang, Seok Joon Won, Jayinee Basu, David Kapfhamer, Raymond A Swanson
Brain injury resulting from stroke or trauma can be exacerbated by the release of proinflammatory cytokines, proteases, and reactive oxygen species by activated microglia. The microglial activation resulting from brain injury is mediated in part by alarmins, which are signaling molecules released from damaged cells. The nuclear enzyme poly(ADP-ribose) polymerase-1 (PARP-1) has been shown to regulate microglial activation after brain injury, and here we show that signaling effects of the alarmin S100B are regulated by PARP-1...
November 2016: Glia
https://www.readbyqxmd.com/read/27339879/caspase-1-deficiency-alleviates-dopaminergic-neuronal-death-via-inhibiting-caspase-7-aif-pathway-in-mptp-p-mouse-model-of-parkinson-s-disease
#5
Chen Qiao, Lin-Xia Zhang, Xi-Yang Sun, Jian-Hua Ding, Ming Lu, Gang Hu
Caspase family has been recognized to be involved in dopaminergic (DA) neuronal death and to exert an unfavorable role in Parkinson's disease (PD) pathology. Our previous study has revealed that caspase-1, as an important component of NLRP3 inflammasome, induces microglia-mediated neuroinflammation in the pathogenesis of PD. However, the role of caspase-1 in DA neuronal degeneration in the onset of PD remains unclear. Here, we showed that caspase-1 knockout ameliorated DA neuronal loss and dyskinesia in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine/probenecid (MPTP/p)-induced PD model mice...
June 23, 2016: Molecular Neurobiology
https://www.readbyqxmd.com/read/27215802/a-diphenyl-diselenide-supplemented-diet-and-swimming-exercise-promote-neuroprotection-reduced-cell-apoptosis-and-glial-cell-activation-in-the-hypothalamus-of-old-rats
#6
Marlon R Leite, José L Cechella, Simone Pinton, Cristina W Nogueira, Gilson Zeni
Aging is a process characterized by deterioration of the homeostasis of various physiological systems; although being a process under influence of multiple factors, the mechanisms involved in aging are not well understood. Here we investigated the effect of a (PhSe)2-supplemented diet (1ppm, 4weeks) and swimming exercise (1% of body weight, 20min per day, 4weeks) on proteins related to glial cells activation, apoptosis and neuroprotection in the hypothalamus of old male Wistar rats (27month-old). Old rats had activation of astrocytes and microglia which was demonstrated by the increase in the levels of glial fibrillary acidic protein (GFAP) and ionized calcium-binding adaptor molecule 1 (Iba-1) in hypothalamus...
September 2016: Experimental Gerontology
https://www.readbyqxmd.com/read/27157545/parp-inhibition-attenuates-early-brain-injury-through-nf-%C3%AE%C2%BAb-mmp-9-pathway-in-a-rat-model-of-subarachnoid-hemorrhage
#7
Ting Chen, Wei Wang, Jian-Ru Li, Hang-Zhe Xu, Yu-Cong Peng, Lin-Feng Fan, Feng Yan, Chi Gu, Lin Wang, Gao Chen
Poly (ADP-ribose) polymerases (PARPs) play an important role in a range of neurological disorders, however, the role of PARP in early brain injury after subarachnoid hemorrhage (SAH) remains unclear. This study was designed to explore the role and the potential mechanisms of PARP in early brain injury after SAH. Eighty-nine male SD rats were randomly divided into the Sham group, SAH+Vehicle group and SAH+PARP inhibitor (PJ34) group. An endovascular perforation model was used to induce SAH in rats. PJ34 (10mg/kg) or vehicle (0...
August 1, 2016: Brain Research
https://www.readbyqxmd.com/read/26637332/nf-%C3%AE%C2%BAb-transcriptional-activation-by-tnf%C3%AE-requires-phospholipase-c-extracellular-signal-regulated-kinase-2-and-poly-adp-ribose-polymerase-1
#8
Billy Vuong, Adam D J Hogan-Cann, Conrad C Alano, Mackenzie Stevenson, Wai Yee Chan, Christopher M Anderson, Raymond A Swanson, Tiina M Kauppinen
BACKGROUND: The nuclear enzyme poly(ADP-ribose) polymerase-1 (PARP-1) is required for pro-inflammatory effects of TNFα. Our previous studies demonstrated that PARP-1 mediates TNFα-induced NF-κB activation in glia. Here, we evaluated the mechanisms by which TNFα activates PARP-1 and PARP-1 mediates NF-κB activation. METHODS: Primary cultures of mouse cortical astrocytes and microglia were treated with TNFα and suitable signaling pathway modulators (pharmacological and molecular)...
December 4, 2015: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/26519900/pharmacology-and-structure-of-p2y-receptors
#9
REVIEW
Ivar von Kügelgen, Kristina Hoffmann
P2Y receptors are G-protein-coupled receptors (GPCRs) for extracellular nucleotides. There are eight mammalian P2Y receptor subtypes (P2Y1, P2Y2, P2Y4, P2Y6, P2Y11, P2Y12, P2Y13, and P2Y14). P2Y receptors are widely expressed and play important roles in physiology and pathophysiology. One important example is the ADP-induced platelet aggregation mediated by P2Y1 and P2Y12 receptors. Active metabolites of the thienopyridine compounds ticlopidine, clopidogrel and prasugrel as well as the nucleoside analogue ticagrelor block P2Y12 receptors and thereby platelet aggregation...
May 2016: Neuropharmacology
https://www.readbyqxmd.com/read/26365310/lrrk2-g2019s-mutation-attenuates-microglial-motility-by-inhibiting-focal-adhesion-kinase
#10
Insup Choi, Beomsue Kim, Ji-Won Byun, Sung Hoon Baik, Yun Hyun Huh, Jong-Hyeon Kim, Inhee Mook-Jung, Woo Keun Song, Joo-Ho Shin, Hyemyung Seo, Young Ho Suh, Ilo Jou, Sang Myun Park, Ho Chul Kang, Eun-Hye Joe
In response to brain injury, microglia rapidly extend processes that isolate lesion sites and protect the brain from further injury. Here we report that microglia carrying a pathogenic mutation in the Parkinson's disease (PD)-associated gene, G2019S-LRRK2 (GS-Tg microglia), show retarded ADP-induced motility and delayed isolation of injury, compared with non-Tg microglia. Conversely, LRRK2 knockdown microglia are highly motile compared with control cells. In our functional assays, LRRK2 binds to focal adhesion kinase (FAK) and phosphorylates its Thr-X-Arg/Lys (TXR/K) motif(s), eventually attenuating FAK activity marked by decreased pY397 phosphorylation (pY397)...
September 14, 2015: Nature Communications
https://www.readbyqxmd.com/read/26200703/recurrent-hypoinsulinemic-hyperglycemia-in-neonatal-rats-increases-parp-1-and-nf-%C3%AE%C2%BAb-expression-and-leads-to-microglial-activation-in-the-cerebral-cortex
#11
Tate Gisslen, Kathleen Ennis, Vineet Bhandari, Raghavendra Rao
BACKGROUND: Hyperglycemia is a common metabolic problem in extremely low-birth-weight preterm infants. Neonatal hyperglycemia is associated with increased mortality and brain injury. Glucose-mediated oxidative injury may be responsible. Poly(ADP-ribose) polymerase-1 (PARP-1) is a nuclear enzyme involved in DNA repair and cell survival. However, PARP-1 overactivation leads to cell death. NF-κB is coactivated with PARP-1 and regulates microglial activation. The effects of recurrent hyperglycemia on PARP-1/NF-κB expression and microglial activation are not well understood...
November 2015: Pediatric Research
https://www.readbyqxmd.com/read/25990044/role-of-toll-like-receptor-4-signaling-pathway-in-the-secondary-damage-induced-by-experimental-spinal-cord-injury
#12
Daniela Impellizzeri, Akbar Ahmad, Rosanna Di Paola, Michela Campolo, Michele Navarra, Emanuela Esposito, Salvatore Cuzzocrea
Toll-like receptors (TLRs) are signaling receptors in the innate immune system that is specific immunologic response to systemic bacterial infection and injury. TLRs contribute to the initial induction of neuroinflammation in the CNS. In spinal cord injury (SCI) intricate immune cell interactions are triggered, typically consisting of a staggered multiphasic immune cell response, which can become deregulated. The present study aims to evaluate the role of TLR4 signaling pathway in the development of secondary damage in a mouse model of SCI using TLR4-deficient (TLR4-KO) mice such as C57BL/10ScNJ and C3H/HeJ mice...
September 2015: Immunobiology
https://www.readbyqxmd.com/read/25847308/different-danger-signals-differently-impact-on-microglial-proliferation-through-alterations-of-atp-release-and-extracellular-metabolism
#13
Jimmy George, Francisco Q Gonçalves, Gonçalo Cristóvão, Lisa Rodrigues, José Roberto Meyer Fernandes, Teresa Gonçalves, Rodrigo A Cunha, Catarina A Gomes
Microglia rely on their ability to proliferate in the brain parenchyma to sustain brain innate immunity and participate in the reaction to brain damage. We now studied the influence of different danger signals activating microglia, both internal (typified by glutamate, associated with brain damage) and external (using a bacterial lipopolysaccharide, LPS), on the proliferation of microglia cells. We found that LPS (100 ng/mL) increased, whereas glutamate (0.5 mM) decreased proliferation. Notably, LPS decreased whereas glutamate increased the extracellular levels of ATP...
September 2015: Glia
https://www.readbyqxmd.com/read/25821842/p2y12-expression-and-function-in-alternatively-activated-human-microglia
#14
Craig S Moore, Ariel R Ase, Angham Kinsara, Vijayaraghava T S Rao, Mackenzie Michell-Robinson, Soo Yuen Leong, Oleg Butovsky, Samuel K Ludwin, Philippe Séguéla, Amit Bar-Or, Jack P Antel
OBJECTIVE: To investigate and measure the functional significance of altered P2Y12 expression in the context of human microglia activation. METHODS: We performed in vitro and in situ experiments to measure how P2Y12 expression can influence disease-relevant functional properties of classically activated (M1) and alternatively activated (M2) human microglia in the inflamed brain. RESULTS: We demonstrated that compared to resting and classically activated (M1) human microglia, P2Y12 expression is increased under alternatively activated (M2) conditions...
April 2015: Neurology® Neuroimmunology & Neuroinflammation
https://www.readbyqxmd.com/read/25689400/sitagliptin-attenuated-brain-damage-and-cognitive-impairment-in-mice-with-chronic-cerebral-hypo-perfusion-through-suppressing-oxidative-stress-and-inflammatory-reaction
#15
Tzu-Hsien Tsai, Cheuk-Kwan Sun, Chai-Hao Su, Pei-Hsun Sung, Sarah Chua, Yen-Yi Zhen, Steve Leu, Hsueh-Wen Chang, Jenq-Lin Yang, Hon-Kan Yip
BACKGROUND: Sitagliptin, a new antidiabetic drug that inhibits dipeptidyl peptidase (DPP)-4 enzyme activity, has been reported to possess neuroprotective property. We tested the protective effects of sitagliptin against chronic cerebral hypoperfusion (CHP) in mice after bilateral carotid artery stenosis (BCAS). METHOD: Thirty C57BL/6 mice were divided into three groups: sham control (n = 10), CHP (n = 10) and CHP-sitagliptin (orally 600 mg/kg/day) (n = 10)...
May 2015: Journal of Hypertension
https://www.readbyqxmd.com/read/25471906/stim1-stim2-and-orai1-regulate-store-operated-calcium-entry-and-purinergic-activation-of-microglia
#16
Marlen Michaelis, Bernhard Nieswandt, David Stegner, Jens Eilers, Robert Kraft
Activation of microglia is the first and main immune response to brain injury. Release of the nucleotides ATP, ADP, and UDP from damaged cells regulate microglial migration and phagocytosis via purinergic P2Y receptors. We hypothesized that store-operated Ca(2+) entry (SOCE), the prevalent Ca(2+) influx mechanism in non-excitable cells, is a potent mediator of microglial responses to extracellular nucleotides. Expression analyses of STIM Ca(2+) sensors and Orai Ca(2+) channel subunits, that comprise the molecular machinery of SOCE, showed relevant levels of STIM1, STIM2, and Orai1 in cultured mouse microglia...
April 2015: Glia
https://www.readbyqxmd.com/read/25186167/p2y13-receptor-mediated-rapid-increase-in-intracellular-calcium-induced-by-adp-in-cultured-dorsal-spinal-cord-microglia
#17
Junwei Zeng, Gaoxia Wang, Xiaohong Liu, Chunmei Wang, Hong Tian, Aidong Liu, Huan Jin, Xiaomei Luo, Yuanshou Chen
P2Y receptors have been implicated in the calcium mobilization by the response to neuroexcitatory substances in neurons and astrocytes, but little is known about P2Y receptors in microglia cells. In the present study, the effects of ADP on the intracellular calcium concentration ([Ca(2+)]i) in cultured dorsal spinal cord microglia were detected with confocal laser scanning microscopy using fluo-4/AM as a calcium fluorescence indicator that could monitor real-time alterations of [Ca(2+)]i. Here we show that ADP (0...
November 2014: Neurochemical Research
https://www.readbyqxmd.com/read/25161822/parp1-enhances-inflammatory-cytokine-expression-by-alteration-of-promoter-chromatin-structure-in-microglia
#18
Ricardo Iván Martínez-Zamudio, Hyo Chol Ha
BACKGROUND: Poly(ADP-ribose) polymerase 1 (PARP1) is a chromatin-associated enzyme that participates in processes such as transcription and DNA repair through the regulation of chromatin structure. Accumulating evidence suggests an important role for PARP1 enzymatic activity in promoting CNS inflammation by facilitating the expression of inflammatory cytokines in glial cells. However, the molecular mechanisms by which PARP1 enzymatic activity mediates this process are not well understood...
July 2014: Brain and Behavior
https://www.readbyqxmd.com/read/25101675/parp1-activation-expression-modulates-regional-specific-neuronal-and-glial-responses-to-seizure-in-a-hemodynamic-independent-manner
#19
J-E Kim, Y-J Kim, J Y Kim, T-C Kang
Poly(ADP-ribose) polymerase-1 (PARP1) plays a regulatory role in apoptosis, necrosis and other cellular processes after injury. Status epilepticus (SE) induces neuronal and astroglial death that show regional-specific patterns in the rat hippocampus and piriform cortex (PC). Thus, we investigated whether PARP1 regulates the differential neuronal/glial responses to pilocarpine (PILO)-induced SE in the distinct brain regions. In the present study, both CA1 and CA3 neurons showed PARP1 hyperactivation-dependent neuronal death pathway, whereas PC neurons exhibited PARP1 degradation-mediated neurodegeneration following SE...
2014: Cell Death & Disease
https://www.readbyqxmd.com/read/25087974/sustained-release-carrier-for-adenosine-triphosphate-as-signaling-molecule
#20
Christian Wischke, Judith Weigel, Larisa Bulavina, Andreas Lendlein
Adenosine triphosphate (ATP) is a molecule with a fascinating variety of intracellular and extracellular biological functions that go far beyond energy metabolism. Due to its limited passive diffusion through biological membranes, controlled release systems may allow to interact with ATP-mediated extracellular processes. In this study, two release systems were explored to evaluate the capacity for either long-term or short-term release: (i) Poly[(rac-lactide)-co-glycolide] (PLGA) implant rods were capable of ATP release over days to weeks, depending on the PLGA molecular weight and end-group capping, but were also associated with partial hydrolytic degradation of ATP to ADP and AMP, but not adenosine...
December 10, 2014: Journal of Controlled Release: Official Journal of the Controlled Release Society
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