Prostaglandin E2 stimulates COX-2 expression via mitogen-activated protein kinase p38 but not ERK in human follicular dendritic cell-like cells.

ABSTRACT:

Background

Prostaglandin E2 (PGE₂) is an endogenous lipid mediator of inflammation. Its production is regulated by the rate-limiting upstream enzyme cyclooxygenase-2 (COX-2). We have recently demonstrated that the major cell type expressing COX-2 in the germinal center is follicular dendritic cell (FDC). In this study, to elucidate the molecular mechanism of PGE₂ in COX-2 production, we asked whether mitogen-activated protein kinases ERK and p38 might regulate COX-2 expression.

Results

FDC-like cells were used to analyze the phosphorylation kinetics of ERK and p38 and the impact of genetic knockdown. PGE₂ stimulation gave rise to a rapid increase of p38 but not ERK phosphorylation. In contrast, IL-1β induced phosphorylation of both MAPKs. Kno

SUBMITTER: Cho W 

PROVIDER: S-EPMC7165408 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature