Differentiation of ob 17 preadipocytes to adipocytes. Effects of prostaglandin F2alpha and relationship to prostaglandin synthesis.

The adipose conversion of ob 17 preadipose cells can be irreversibly blocked when prostaglandin F2alpha is included post-confluence for a minimum of 24 h in insulin-containing media. Prostaglandins E1 and E2 are inactive. The lack of adipose conversion is accompanied by the maintenance of a fusiform cell shape, by a slow increase in cell number and by a potent rise in de novo prostaglandin synthesis; it is paralleled by the absence of the characteristic phenotypes of adipose conversion. The multiple effects of prostaglandin F2alpha are dose-dependent, with half-maximal concentrations ranging from 10 to 40 nM. The absence of differentiation and the high rate of prostaglandin synthesis in the presence of prostaglandin F2alpha are likely a consequence of a sustained growth, as also observed with other growth-promoting agents (bovine retinal extract and cat serum). Indomethacin, while suppressing endogenous prostaglandin synthesis, is unable to reverse the long-term and multiple effects of prostaglandin F2alpha. Although adipose conversion normally follows a decrease in prostaglandin production (R. Négrel and G. Ailhaud, Biochem. Biophys. Res. Commun. (1981) 98, 768-777), these results indicate that both events can be dissociated.