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J. Biol. Chem., Vol. 277, Issue 36, 32992-33000, September 6, 2002
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From the University of Iowa Roy J. and Lucille A. Carver College
of Medicine and Veterans Administration Medical Center, Iowa City,
Iowa 52242
Human alveolar macrophages have both
lipopolysaccharide (LPS)-induced and constitutive
phosphatidylinositol 3-kinase (PI3K) activity. We observed
that blocking PI3K activity increased release of prostaglandin
E2 after LPS exposure, and increasing PI3K activity (interleukin-13) decreased release of prostaglandin E2 after LPS exposure. This was not because of an effect of PI3K on phospholipase 2 activity. PI3K inhibition resulted in an increase in cyclooxygenase 2 (COX2) protein, mRNA, and mRNA stability. PI3K negatively
regulated activation of the p38 pathway (p38, MKK3/6, and
MAPKAP2), and an active p38 was necessary for COX2 production. The data
suggest that PI3K inhibition of p38 modulates COX2 expression via
destabilization of LPS-induced COX2 mRNA.
Phosphatidylinositol 3-Kinase Activity Negatively
Regulates Stability of Cyclooxygenase 2 mRNA*
,
*
This work was supported in part by a Veterans Administration
Merit Review grant, National Institutes of Health Grants HL-60316 and
ES-09607, Environmental Protection Agency Grant R826711 (to G. W. H.), National Institutes of Health Grant HL-03860 (to
A. B. C.), and Grant RR00059 from the General Clinical Research
Centers Program, NCRR, National Institutes of Health.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Division of Pulmonary,
Critical Care, and Occupational Medicine, Rm. 100, EMRB, University of
Iowa Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA
52242. Tel.: 319-335-7590; Fax: 319-335-6530; E-mail: martha-monick@uiowa.edu.
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