Phosphatidylinositol 3-kinase activity negatively regulates stability of cyclooxygenase 2 mRNA

83Citations
Citations of this article
26Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

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.

Cite

CITATION STYLE

APA

Monick, M. M., Robeff, P. K., Butler, N. S., Flaherty, D. M., Brent Carter, A., Peterson, M. W., & Hunninghake, G. W. (2002). Phosphatidylinositol 3-kinase activity negatively regulates stability of cyclooxygenase 2 mRNA. Journal of Biological Chemistry, 277(36), 32992–33000. https://doi.org/10.1074/jbc.M203218200

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free