The mechanism of inhibition of 3T3-L1 preadipocyte differentiation by prostaglandin F2alpha

Endocrinology
C W MillerJ M Ntambi

Abstract

We have shown previously that treatment of 3T3-L1 preadipocytes with prostaglandin F2alpha (PGF2alpha) and fluprostenol, a prostanoid FP2 receptor (FP receptor) agonist, inhibited adipocyte differentiation. In this study, we demonstrate that the inhibition by PGF2alpha is controlled by concentrations of PGF2alpha rather than regulation of FP receptor levels or binding. Membranes prepared from either 3T3-L1 preadipocytes or adipocytes exhibited specific binding for PGF2alpha, suggesting that FP receptors are present throughout differentiation. Endogenous PGF2alpha production in 3T3-L1s was lower in differentiating cells compared with uninduced preadipocytes, providing further evidence that regulation occurs at the level of ligand concentration. Stimulation of the FP receptor causes a transient intracellular calcium increase, an activation of a calcium/calmodulin-dependent protein kinase (CaMK), and an increase in DNA synthesis, associated with the inhibition of differentiation. Calcium mobilizing agents, A23187 and thapsigargin, mimic the FP receptor-induced inhibition of differentiation, suggesting a role for calcium. KN-62, a CaMK inhibitor, reversed the inhibition of differentiation when added to differentiating cells with fl...Continue Reading

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