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Plasminogen-induced IL-1beta and TNF-alpha production in microglia is regulated by reactive oxygen species.

Min, KJ; Jou, I; Joe, E
Biochemical and biophysical research communications, 312(4):969-974, 2003
Journal Title
Biochemical and biophysical research communications
Microglia, major immune effector cells in the central nervous system, become activated during brain injury. In this study we showed that the blood component plasminogen/plasmin activates microglia. Plasminogen-induced IL-1beta, TNF-alpha, and iNOS mRNA expression in primary cultured rat microglia and BV2 murine microglial cells. Plasmin caused a similar response. Serine protease inhibitors suppressed both plasminogen- and plasmin-induced IL-1beta and TNF-alpha expression, indicating the importance of serine protease activity in plasminogen/plasmin activation of microglia. Reactive oxygen species (ROS) appeared to play an important role in plasminogen-induced microglial activation, with ROS being generated within 15min of plasminogen treatment, and antioxidants (100 microM trolox and 10mM NAC) reducing IL-1beta and TNF-alpha expression in plasminogen-treated cells. Furthermore, plasminogen stimulated CREB and NF-kappaB DNA binding activity, and this activation was also reduced by trolox and NAC. These results suggest that plasminogen activates microglia via stimulation of ROS production.
MeSH terms
AnimalsCell LineCells, CulturedDose-Response Relationship, DrugFibrinolysin/metabolism*Fibrinolysin/pharmacologyGene Expression Regulation/drug effectsGene Expression Regulation/physiologyHomeostasis/drug effectsHomeostasis/physiologyInterleukin-1/biosynthesis*MiceMicroglia/drug effectsMicroglia/metabolism*Nitric Oxide Synthase/biosynthesis*Nitric Oxide Synthase Type IIPlasminogen/metabolism*Plasminogen/pharmacologyRatsRats, Sprague-DawleyReactive Oxygen Species/metabolism*Tumor Necrosis Factor-alpha/biosynthesis*
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
AJOU Authors
주, 일로조, 은혜
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