Cited 31 time in webofscience Cited 34 time in scopus

Translocator Protein 18 kDa Negatively Regulates Inflammation in Microglia

Title
Translocator Protein 18 kDa Negatively Regulates Inflammation in Microglia
Authors
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
2014-06
Citation
Journal of Neuroimmune Pharmacology, 9(3), 424-437
Type
Article
Article Type
Article
Keywords
4 Aminobutyric Acid ReceptorAnimalAnimal CellAnimal ExperimentAnimal ModelAnimalsAutacoidBeta ActinBrain RegionBzrp Protein, MouseC57Bl MouseCell LineCentral Nervous SystemControlled StudyCytokineCytokine ProductionDegenerative DiseaseGene ExpressionImmunologyInducible Nitric Oxide SynthaseInflammationInflammation MediatorsInterleukin-6LipopolysaccharideMaleMetabolismMiceMice, Inbred C57BLMicrogliaMitochondrial ProteinMouseNerve Cell NecrosisNervous System InflammationNeurodegenerationNeuroinflammationNF-Kappa BNon-HumanOuter Membrane ProteinPathologyPathophysiologyPhysiologyPriority JournalProtein ExpressionReceptor Activator of Nuclear Factor Kappa BReceptors, GabaRegulatory MechanismSignal TransductionTranslocator Protein18 kDaTumor Necrosis Factor-AlphaUnclassified DrugUpregulation
ISSN
1557-1890
Abstract
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.
URI
http://hdl.handle.net/20.500.11750/2390
DOI
10.1007/s11481-014-9540-6
Publisher
Springer
Related Researcher
Files:
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Collection:
Brain and Cognitive SciencesLaboratory of Neuronal Cell Death1. Journal Articles


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