Microglial Activation in Neuroinflammation: Implications for the Etiology of Neurodegeneration
Background: Activated microglia secrete inflammatory cytokines and may play roles in the progression of neurodegenerative diseases. However, the mechanism underlying microglial activation remains unclear. Objective: Our aim was to examine the regulation of activated microglia through their cell deat...
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Published in | Neuro-degenerative diseases Vol. 10; no. 1-4; pp. 100 - 103 |
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Main Authors | , , , , , |
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Language | English |
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Basel, Switzerland
S. Karger AG
01.01.2012
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Abstract | Background: Activated microglia secrete inflammatory cytokines and may play roles in the progression of neurodegenerative diseases. However, the mechanism underlying microglial activation remains unclear. Objective: Our aim was to examine the regulation of activated microglia through their cell death and survival pathways. Methods: We used mouse primary-cultured microglia, which are destined to die within a few days under ordinary culture conditions. The microglia live for longer than 1 month, without any measurable increase in apoptotic or necrotic cell death, when kept activated by sublethal concentrations of lipopolysaccharide (LPS). Results: LPS-treated microglia showed changes in shape. LPS treatment had no effect on the level of the proapoptotic Bcl-2-associated X protein but increased the level of the antiapoptotic protein Bcl-xL at day 1. Furthermore, the level of microtubule-associated light chain 3-II, a marker protein for autophagy, was decreased 3 h after exposure to LPS.Conclusion:An increase in Bcl-xL seems to inhibit both apoptosis and autophagy. Our results suggest that long-lived microglia resulting from exposure to the optimal dose of LPS may play critical roles in the progression of neurodegeneration. |
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AbstractList | Activated microglia secrete inflammatory cytokines and may play roles in the progression of neurodegenerative diseases. However, the mechanism underlying microglial activation remains unclear.
Our aim was to examine the regulation of activated microglia through their cell death and survival pathways.
We used mouse primary-cultured microglia, which are destined to die within a few days under ordinary culture conditions. The microglia live for longer than 1 month, without any measurable increase in apoptotic or necrotic cell death, when kept activated by sublethal concentrations of lipopolysaccharide (LPS).
LPS-treated microglia showed changes in shape. LPS treatment had no effect on the level of the proapoptotic Bcl-2-associated X protein but increased the level of the antiapoptotic protein Bcl-xL at day 1. Furthermore, the level of microtubule-associated light chain 3-II, a marker protein for autophagy, was decreased 3 h after exposure to LPS.
An increase in Bcl-xL seems to inhibit both apoptosis and autophagy. Our results suggest that long-lived microglia resulting from exposure to the optimal dose of LPS may play critical roles in the progression of neurodegeneration. BACKGROUNDActivated microglia secrete inflammatory cytokines and may play roles in the progression of neurodegenerative diseases. However, the mechanism underlying microglial activation remains unclear.OBJECTIVEOur aim was to examine the regulation of activated microglia through their cell death and survival pathways.METHODSWe used mouse primary-cultured microglia, which are destined to die within a few days under ordinary culture conditions. The microglia live for longer than 1 month, without any measurable increase in apoptotic or necrotic cell death, when kept activated by sublethal concentrations of lipopolysaccharide (LPS).RESULTSLPS-treated microglia showed changes in shape. LPS treatment had no effect on the level of the proapoptotic Bcl-2-associated X protein but increased the level of the antiapoptotic protein Bcl-xL at day 1. Furthermore, the level of microtubule-associated light chain 3-II, a marker protein for autophagy, was decreased 3 h after exposure to LPS.CONCLUSIONAn increase in Bcl-xL seems to inhibit both apoptosis and autophagy. Our results suggest that long-lived microglia resulting from exposure to the optimal dose of LPS may play critical roles in the progression of neurodegeneration. Background: Activated microglia secrete inflammatory cytokines and may play roles in the progression of neurodegenerative diseases. However, the mechanism underlying microglial activation remains unclear. Objective: Our aim was to examine the regulation of activated microglia through their cell death and survival pathways. Methods: We used mouse primary-cultured microglia, which are destined to die within a few days under ordinary culture conditions. The microglia live for longer than 1 month, without any measurable increase in apoptotic or necrotic cell death, when kept activated by sublethal concentrations of lipopolysaccharide (LPS). Results: LPS-treated microglia showed changes in shape. LPS treatment had no effect on the level of the proapoptotic Bcl-2-associated X protein but increased the level of the antiapoptotic protein Bcl-xL at day 1. Furthermore, the level of microtubule-associated light chain 3-II, a marker protein for autophagy, was decreased 3 h after exposure to LPS.Conclusion:An increase in Bcl-xL seems to inhibit both apoptosis and autophagy. Our results suggest that long-lived microglia resulting from exposure to the optimal dose of LPS may play critical roles in the progression of neurodegeneration. Background: Activated microglia secrete inflammatory cytokines and may play roles in the progression of neurodegenerative diseases. However, the mechanism underlying microglial activation remains unclear. Objective: Our aim was to examine the regulation of activated microglia through their cell death and survival pathways. Methods: We used mouse primary-cultured microglia, which are destined to die within a few days under ordinary culture conditions. The microglia live for longer than 1 month, without any measurable increase in apoptotic or necrotic cell death, when kept activated by sublethal concentrations of lipopolysaccharide (LPS). Results: LPS-treated microglia showed changes in shape. LPS treatment had no effect on the level of the proapoptotic Bcl-2-associated X protein but increased the level of the antiapoptotic protein Bcl-xL at day 1. Furthermore, the level of microtubule-associated light chain 3-II, a marker protein for autophagy, was decreased 3 h after exposure to LPS.Conclusion:An increase in Bcl-xL seems to inhibit both apoptosis and autophagy. Our results suggest that long-lived microglia resulting from exposure to the optimal dose of LPS may play critical roles in the progression of neurodegeneration. Copyright © 2012 S. Karger AG, Basel [PUBLICATION ABSTRACT] |
Author | Nakashima, Akira Nagatsu, Toshiharu Kaneko, Yoko S. Mori, Keiji Nagatsu, Ikuko Ota, Akira |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22301667$$D View this record in MEDLINE/PubMed |
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Keywords | Lipopolysaccharide Life span Autophagy Apoptosis Microglia |
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References | Mizushima N, Levine B, Cuervo AM, Klionsky DJ: Autophagy fights disease through cellular self-digestion. Nature 2008;451:1069–1075.1830553810.1038%2Fnature06639 Nagatsu T, Sawada M: Cellular and molecular mechanisms of Parkinson’s disease: neurotoxins, causative genes, and inflammatory cytokines. Cell Mol Neurobiol 2006;26:781–802.1682362510.1007%2Fs10571-006-9061-9 Hara T, Nakamura K, Matsui M, Yamamoto A, Nakahara Y, Suzuki-Migishima R, Yokoyama M, Mishima K, Saito I, Okano H, Mizushima N: Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice. Nature 2006;441:885–889.1662520410.1038%2Fnature04724 Komatsu M, Waguri S, Chiba T, Murata S, Iwata J, Tanida I, Ueno T, Koike M, Uchiyama Y, Kominami E, Tanaka K: Loss of autophagy in the central nervous system causes neurodegeneration in mice. Nature 2006;441:880–884.1662520510.1038%2Fnature04723 Kaneko YS, Nakashima A, Mori K, Nagatsu T, Nagatsu I, Ota A: Lipopolysaccharide extends the lifespan of mouse primary-cultured microglia. Brain Res 2009;1279:9–20.10.1016%2Fj.brainres.2009.05.008 Islam S, Hassan F, Tumurkhuu G, Ito H, Koide N, Mori I, Yoshida T, Yokochi T: Lipopolysaccharide prevents apoptosis induced by brefeldin A, an endoplasmic reticulum stress agent, in RAW 264.7 cells. Biochem Biophys Res Commun 2006;340:589–596.10.1016%2Fj.bbrc.2005.12.050 Cho BP, Song DY, Sugama S, Shin DH, Shimizu Y, Kim SS, Kim YS, Joh TH: Pathological dynamics of activated microglia following medial forebrain bundle transection. Glia 2006;53:92–102.10.1002%2Fglia.20265 Halliday GM, Stevens CH: Glia: initiators and progressors of pathology in Parkinson’s disease. Mov Disord 2011;26:6–17.10.1002%2Fmds.23455 Xu Y, Jagannath C, Liu X-D, Sharafkhaneh A, Kolodziejska KE, Eissa NT: Toll-like receptor 4 is a sensor for autophagy associated with innate immunity. Immunity 2007;27:135–144.1765827710.1016%2Fj.immuni.2007.05.022 McCarty MF: Down-regulation of microglial activation may represent a practical strategy for combating neurodegenerative disorders. Med Hypotheses 2006;67:251–269.1651328710.1016%2Fj.mehy.2006.01.013 Levine B: Eating oneself and uninvited guests: autophagy-related pathways in cellular defense. Cell 2005;120:159–162.15680321 Wang J-Y, Yang J-M, Wang J-Y, Tao P-L, Yang SN: Synergistic apoptosis induced by bacterial endotoxin lipopolysaccharide and high glucose in rat microglia. Neurosci Lett 2001;304:177–180.10.1016%2FS0304-3940%2801%2901780-3 Naert G, Rivest S: The role of microglial cell subsets in Alzheimer’s disease. Curr Alzheimer Res 2011;8:151–155. Block ML, Hong JS: Microglia and inflammation-mediated neurodegeneration: multiple triggers with a common mechanism. Prog Neurobiol 2005;76:77–98.10.1016%2Fj.pneurobio.2005.06.004 Kabeya Y, Mizushima N, Ueno T, Yamamoto A, Kirisako T, Noda T, Kominami E, Ohsumi Y, Yoshimori T: LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing. EMBO J 2000;19:5720–5728.1106002310.1093%2Femboj%2F19.21.5720 Howell OW, Rundle JL, Garg A, Komada M, Brophy PJ, Reynolds R: Activated microglia mediate axoglial disruption that contributes to axonal injury in multiple sclerosis. J Neuropathol Exp Neurol 2010;69:1017–1033.10.1097%2FNEN.0b013e3181f3a5b1 Kaneko YS, Mori K, Nakashima A, Sawada M, Nagatsu I, Ota A: Peripheral injection of lipopolysaccharide enhances expression of inflammatory cytokines in murine locus coeruleus: possible role of increased norepinephrine turnover. J Neurochem 2005;94:393–404.1599829010.1111%2Fj.1471-4159.2005.03209.x Mizushima N: Autophagy: process and function. Genes Dev 2007;21:2861–2873.1800668310.1101%2Fgad.1599207 Tsujimoto Y: Role of Bcl-2 family proteins in apoptosis: apoptosomes or mitochondria? Genes Cells 1998;3:697–707.999050510.1046%2Fj.1365-2443.1998.00223.x Liu B, Wang K, Gao HM, Mandavilli B, Wang JY, Hong JS: Molecular consequences of activated microglia in the brain: overactivation induces apoptosis. J Neurochem 2001;77:182–189.1127927410.1046%2Fj.1471-4159.2001.t01-1-00216.x ref13 ref12 ref15 ref14 ref11 ref10 ref2 ref1 ref17 ref16 ref18 ref8 ref7 ref9 ref4 ref3 ref6 ref5 |
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Snippet | Background: Activated microglia secrete inflammatory cytokines and may play roles in the progression of neurodegenerative diseases. However, the mechanism... Activated microglia secrete inflammatory cytokines and may play roles in the progression of neurodegenerative diseases. However, the mechanism underlying... BACKGROUNDActivated microglia secrete inflammatory cytokines and may play roles in the progression of neurodegenerative diseases. However, the mechanism... |
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SubjectTerms | Animals Apoptosis - drug effects Apoptosis - physiology bcl-2-Associated X Protein - metabolism bcl-X Protein - metabolism Brain - cytology Caspase 3 - metabolism Cells, Cultured Cytokines - metabolism Lipopolysaccharides - pharmacology Mice Microglia - drug effects Signal Transduction - drug effects |
Title | Microglial Activation in Neuroinflammation: Implications for the Etiology of Neurodegeneration |
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