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Expression of a constitutively active form of phosphatidylinositol 3‐kinase inhibits the induction of nitric oxide synthase in human astrocytes
Author(s) -
Pahan Kalipada,
Liu Xiaojuan,
Wood Charles,
Raymond John R.
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)01465-4
Subject(s) - nitric oxide synthase , phosphatidylinositol , nitric oxide , kinase , chemistry , microbiology and biotechnology , proinflammatory cytokine , biology , immunology , inflammation , organic chemistry
The present study underlines the importance of phosphatidylinositol 3‐kinase (PI 3‐kinase) in attenuating the induction of nitric oxide synthase (iNOS) in human astrocytes. Proinflammatory cytokines induced the production of nitric oxide (NO) and the expression of iNOS in human U373MG astrocytoma cells and primary astrocytes. Expression of a catalytically active p110 subunit (p110*) of PI 3‐kinase but not that of a kinase‐deficient mutant of p110 (p110‐kd) induced an increase in PI 3‐kinase activity and inhibited cytokine‐induced production of NO and expression of iNOS. However, expression of p110* had no effect on the activation of NF‐kB, suggesting that p110* inhibits the expression of iNOS without inhibiting the activation of NF‐kB.