Interactions between the transforming growth factor beta (TGF beta) and retinoic acid signal transduction pathways in murine embryonic palatal cells

• Published in: Differentiation (London) Vol. 58; no. 2; p. 149
• Main Authors: Nugent, P, Greene, R M
• Format: Journal Article
• Language: English
• Published: England 01-12-1994
• Subjects: Animals; Blotting, Northern; Cells, Cultured; Gene Expression Regulation - drug effects; Gene Expression Regulation - physiology; Growth Substances - physiology; Mice; Palate - embryology; Receptors, Retinoic Acid - biosynthesis; Signal Transduction - physiology; Transforming Growth Factor beta - biosynthesis; Transforming Growth Factor beta - physiology; Tretinoin - pharmacology
• ISSN: 0301-4681

Regulation of expression of transforming growth factor-beta 3 (TGF-beta 3) and the cellular retinoic acid-binding proteins-I and II (CRABP-I, -II) by retinoic acid (RA) and TGF-beta was examined in primary cultures of murine embryonic palate mesenchymal (MEPM) cells. Northern blot hybridization revealed that RA and TGF-beta 1, beta 2 and beta 3 stimulated the expression of TGF-beta 3 mRNA within 24 hours of treatment. RA down-regulated the expression of CRABP-I mRNA and up-regulated the expression of CRABP-II mRNA in a time- and dose-dependent fashion. TGF-beta 1, beta 2 and beta 3 also down-regulated the expression of CRABP-I mRNA, while epidermal growth factor (EGF) and transforming growth factor alpha (TGF-alpha) were without effect. TGF-beta 1 also stimulated a dose-dependent increase in the expression of CRABP-II mRNA. Again EGF and TGF-alpha were without effect. Basic fibroblast growth factor (bFGF) elicited a slight inhibitory effect on CRABP-II and a slight stimulatory effect on CRABP-I mRNA expression. Thus, cells derived from the mammalian developing palate express CRABP-I and CRABP-II mRNAs, both of which may be regulated by RA and TGF-beta. These data constitute the first demonstration of an effect of TGF-beta on the expression of CRABP-I and CRABP-II and provide further evidence for cross-talk between RA and TGF-beta signal transduction pathways.