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Requirement of Retinoic Acid Receptor Isotypes , ß, and during the Initial Steps of Neural Differentiation of PCC7 Cells

Institute of Physiological Chemistry and Pathobiochemistry, Johannes Gutenberg-University, Medical School, 55099 Mainz, Germany

Address all correspondence and requests for reprints to: Christina Zechel, Institute of Physiological Chemistry and Pathobiochemistry, Johannes Gutenberg-University, Medical School, Duesberg Weg 6, 55099 Mainz, Germany. E-mail: zechel{at}uni-mainz.de.

Retinoic acid (RA) is indispensable for morphogenesis and differentiation of several tissues, including the nervous system. The requirement of the RA receptor (RAR) isotypes , ß, and and the putative role of retinoid X receptor-(RXR) signaling in RA-induced neural differentiation, was analyzed. For this compound-selective retinoids and the murine embryonal carcinoma cell line PCC7, a model system for RA-dependent neural differentiation was used. The present paper shows that proliferating PCC7 cells primarily express RXR and RAR, lower levels of RXRß, and barely detectable amounts of RARß, RAR, and RXR. At receptor-selective concentrations, only a RAR or RAR agonist induced the typical tissue-like differentiation pattern consisting of neuronal and nonneuronal cells. Differentiation-associated processes, such as the down-regulation of Oct4, up-regulation of certain nuclear receptors and proneuronal genes, and the induction of neuronal markers could be triggered by receptor-selective concentrations of a RAR-, ß-, or -selective agonist, although with distinct efficacy. The differences are only partially explained by the distinct RAR, ß, and expression levels and the dissociation constants for the bound retinoids, suggesting differential requirement of RAR isotypes during the initial stages of neural differentiation of PCC7 cells.

NURSA Molecule Pages Link:

Nuclear Receptors:   RARα  |  RARβ  |  RARγ  |  RXRα

Coregulators:   GRIP1  |  NCOR  |  SMRT

Ligands:   Am 580  |  all-trans-Retinoic acid  |  9-cis-Retinoic acid

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