Title |
Pharmacological inhibition of Akt and downstream pathways modulates the expression of COX-2 and mPGES-1 in activated microglia
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Published in |
Journal of Neuroinflammation, January 2012
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DOI | 10.1186/1742-2094-9-2 |
Pubmed ID | |
Authors |
Antonio CP de Oliveira, Eduardo Candelario-Jalil, Julia Langbein, Lena Wendeburg, Harsharan S Bhatia, Johannes CM Schlachetzki, Knut Biber, Bernd L Fiebich |
Abstract |
Microglia are considered a major target for modulating neuroinflammatory and neurodegenerative disease processes. Upon activation, microglia secrete inflammatory mediators that contribute to the resolution or to further enhancement of damage in the central nervous system (CNS). Therefore, it is important to study the intracellular pathways that are involved in the expression of the inflammatory mediators. Particularly, the role of the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) and glycogen synthase kinase-3 (GSK-3) pathways in activated microglia is unclear. Thus, in the present study we investigated the role of Akt and its downstream pathways, GSK-3 and mTOR, in lipopolysaccharide (LPS)-activated primary rat microglia by pharmacological inhibition of these pathways in regard to the expression of cyclooxygenase (COX)-2 and microsomal prostaglandin E synthase-1 (mPGES-1) and to the production of prostaglandin (PG) E2 and PGD2. |
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Geographical breakdown
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Spain | 1 | 1% |
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Unknown | 65 | 96% |
Demographic breakdown
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Student > Ph. D. Student | 9 | 13% |
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Professor > Associate Professor | 6 | 9% |
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