Salazar-Olivo L A, Castro-Muñozledo F, de la Garza M, Kuri-Harcuch W
Depto. de Biología Celular, Centro de Investigación y de Estudios Avanzados del I.P.N., México D.F., Mexico.
Biochem Biophys Res Commun. 1994 Oct 14;204(1):257-63. doi: 10.1006/bbrc.1994.2453.
Retinoic acid (RA) inhibits 3T3 adipogenesis in a dose-dependent and reversible manner, but its mechanism of action remains unknown. 3T3-F442A cell variants obtained by mutagenesis with nitrosoguanidine and/or selection with high RA concentrations showed different resistance to RA cytotoxicity and underwent adipose conversion of various extents when they were cultured in adipogenic conditions. Commitment to adipose differentiation was also inhibited by RA in these clones. Gel filtration chromatography showed the presence of a cytosolic RA-binding activity in the parental cells but not in three of the variant clones isolated. We demonstrate that cytoplasmic RA-binding activity is not essential for the inhibitory effects of the retinoid on 3T3 adipogenesis, or for resistance to RA cytotoxicity. Other mechanisms should be involved to explain the inhibition of adipose differentiation by RA.
