Transglutaminase 2 induces nitric oxide synthesis in BV-2 microglia
Autor: | Tong H. Joh, Kyung Cheon Chung, Jong Min Lee, Key Chung Park, Yoon Seong Kim, Soo-Youl Kim |
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Rok vydání: | 2004 |
Předmět: |
Lipopolysaccharides
Lipopolysaccharide Tissue transglutaminase Biophysics Inflammation Nitric Oxide Biochemistry Cell Line Nitric oxide Mice chemistry.chemical_compound Enzyme activator GTP-Binding Proteins medicine Animals Protein Glutamine gamma Glutamyltransferase 2 Molecular Biology Transglutaminases Dose-Response Relationship Drug Indoleacetic Acids integumentary system Microglia biology Neurodegeneration Cell Biology medicine.disease Cell biology Enzyme Activation Nitric oxide synthase medicine.anatomical_structure chemistry biology.protein medicine.symptom |
Zdroj: | Biochemical and Biophysical Research Communications. 323:1055-1062 |
ISSN: | 0006-291X |
DOI: | 10.1016/j.bbrc.2004.08.204 |
Popis: | A hallmark of brain inflammation is the activation of microglia. Excessive production of nitric oxide (NO), as a consequence of increased inducible nitric oxide synthase (iNOS) in glia, contributes to neurodegeneration. Transglutaminase 2 (TGase 2) is a cross-linking enzyme, which is increased in neurodegeneration. TGase 2 is also considered to be a useful and reliable marker for activation levels in resident and inflammatory macrophages. Therefore, an increase of TGase 2 expression may contribute to activation of microglia. To test this hypothesis, we analyzed the expression of TGase 2 in BV-2 microglia activated with lipopolysaccharide (LPS). Total TGase activity was increased about 5-fold after 24h exposure to LPS. The increase of NO synthesis is correlated with increase of TGase 2 expression. Secretion of NO was reduced between 40 and 80% by TGase inhibition in a dose-dependent manner. This suggests that TGase 2 appears to control iNOS transcription. |
Databáze: | OpenAIRE |
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