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Attenuation of Translocator Protein 18 kDa (TSPO) Up-Regulation by Peroxisome Proliferator-Activated Receptor γ Ligand in Activated Microglia
- Attenuation of Translocator Protein 18 kDa (TSPO) Up-Regulation by Peroxisome Proliferator-Activated Receptor γ Ligand in Activated Microglia
- Shim, Hyun Jung; Yu, Seong Woon; Cho, Hyo Jin
- DGIST Authors
- Yu, Seong Woon
- Issue Date
- Quantitative Bio-Science, 33(1), 41-45
- Microglia; Neuroinflammation; PPARγ; Translocator protein 18 kDa (TSPO)
- Translocator protein (18 kDa) (TSPO) is a five transmembrane domain protein localized primarily in the outer mitochondrial membrane. Recently, we reported that TSPO is a negative regulator of neuroinflammation in microglia. Peroxisome proliferator-activated receptor (PPAR) is a ligand-specific transcriptional factor belonging to the nuclear receptor superfamily and predicted as a putative TSPO transcriptional factor. A number of studies suggest that the activation of PPARhas anti-inflammatory effects. In this study, we observed that treatment of rosiglitazone, a PPARligand significantly decreased the NO production in lipopolysaccharide-stimulated BV2 microglia cell, indicating inhibition of microglial activation. The inhibitory effect of rosiglitazone extended to attenuated protein level of TSPO. TSPO up-regulation seems an adaptive anti-inflammatory response to overcome microglia activation, according to our previous report. Taken together, these results indicate that PPARactivation by rosiglitazone attenuates neuroinflammation and leads to reduced expression of TSPO in the BV2 microglial cells.
- 계명대학교 자연과학연구소
- Related Researcher
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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