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Translocator Protein 18 kDa Negatively Regulates Inflammation in Microglia
- Translocator Protein 18 kDa Negatively Regulates Inflammation in Microglia
- Bae, KR[Bae, Keun-Ryung]; Shim, HJ[Shim, Hyun-Jung]; Balu, D[Balu, Deebika]; Kim, SR[Kim, Sang Ryong]; Yu, SW[Yu, Seong-Woon]
- DGIST Authors
- Bae, KR[Bae, Keun-Ryung]; Shim, HJ[Shim, Hyun-Jung]; Kim, SR[Kim, Sang Ryong]; Yu, SW[Yu, Seong-Woon]
- Issue Date
- Journal of Neuroimmune Pharmacology, 9(3), 424-437
- Article Type
- 4 Aminobutyric Acid Receptor; Animal; Animal Cell; Animal Experiment; Animal Model; Animals; Autacoid; Beta Actin; Brain Region; Bzrp Protein, Mouse; C57Bl Mouse; Cell Line; Central Nervous System; Controlled Study; Cytokine; Cytokine Production; Degenerative Disease; Gene Expression; Immunology; Inducible Nitric Oxide Synthase; Inflammation; Inflammation Mediators; Interleukin-6; Lipopolysaccharide; Male; Metabolism; Mice; Mice, Inbred C57BL; Microglia; Mitochondrial Protein; Mouse; Nerve Cell Necrosis; Nervous System Inflammation; Neurodegeneration; Neuroinflammation; NF-Kappa B; Non-Human; Outer Membrane Protein; Pathology; Pathophysiology; Physiology; Priority Journal; Protein Expression; Receptor Activator of Nuclear Factor Kappa B; Receptors, Gaba; Regulatory Mechanism; Signal Transduction; Translocator Protein18 kDa; Tumor Necrosis Factor-Alpha; Unclassified Drug; Upregulation
- Translocator protein 18 kDa (TSPO) is a mitochondrial outer membrane protein. Although TSPO expression is up-regulated during neuroinflammation, the role of TSPO and its signaling mechanisms in regulation of neuroinflammation remains to be elucidated at the molecular level. Here we demonstrate that TSPO is a negative regulator of neuroinflammation in microglia. Over-expression of TSPO decreased production of pro-inflammatory cytokines upon lipopolysaccharide treatment while TSPO knock-down had the opposite effect. Anti-inflammatory activity of TSPO is also supported by increased expression of alternatively activated M2 stage-related genes. These data suggest that up-regulation of TSPO level during neuroinflammation may be an adaptive response mechanism. We also provide the evidence that the repressive activity of TSPO is at least partially mediated by the attenuation of NF-κB activation. Neurodegenerative diseases are characterized by loss of specific subsets of neurons at the particular anatomical regions of the central nervous system. Cause of neuronal death is still largely unknown, but it is becoming clear that neuroinflammation plays a significant role in the pathophysiology of neurodegenerative diseases. Understanding the mechanisms underlying the inhibitory effects of TSPO on neuroinflammation can contribute to the therapeutic design for neurodegenerative diseases. © 2014 Springer Science+Business Media.
- Related Researcher
Yu, Seong Woon
Laboratory of Neuronal Cell Death
Molecular mechanisms of neuronal cell death and neurodegeneration
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- Department of Brain and Cognitive SciencesLaboratory of Neuronal Cell Death1. Journal Articles
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