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Antisense Oligonucleotides to CRABP I and II Alter the Expression of TGF-p3, RAR-β, and Tenascin in Primary Cultures of Embryonic Palate Cells

Paul Nugent and Robert M. Greene
In Vitro Cellular & Developmental Biology. Animal
Vol. 31, No. 7 (Jul. - Aug., 1995), pp. 553-558
Stable URL: http://www.jstor.org/stable/4294465
Page Count: 6
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Antisense Oligonucleotides to CRABP I and II Alter the Expression of TGF-p3, RAR-β, and Tenascin in Primary Cultures of Embryonic Palate Cells
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Abstract

The cellular retinoic acid-binding proteins (CRABPs) are thought to modulate the responsiveness of cells to retinoic acid (RA). We have previously shown that primary cultures of murine embryonic palate mesenchymal (MEPM) cells express both CRABP-I and CRABP-II genes and that this expression is regulated by RA and transforming growth factor β (TGF-β). These cells also express high levels of TGF-β3, which is also regulated by RA and TGF-β. We have used an antisense strategy to investigate the role of the CRABPs in retinoid-induced gene expression. Subconfluent cultures of MEPM cells were treated for several days with phosphorothioate modified 18-mer oligonucleotides antisense to CRABP-I or CRABP-II and then with all-trans-retinoic acid at a concentration of 3.3 µM or 0.33 µM for 5 or 22 h. Total RNA was then extracted and the expression of TGF-β3, retinoic acid receptor β (RAR-β), and tenascin was assessed by northern blot analysis. Antisense oligonucleotides to CRABP-I partially inhibited the RA-induced TGF-β3, RAR-β, and tenascin mRNA expression. The corresponding mis-sense oligonucleotides were without effect. Antisense oligonucleotides to CRABP-II also partially inhibited RA-induced expression of these genes. As with the CRABP-I antisense, mis-sense oligonucleotides to CRABP-II had no effect. These data suggest that both CRABPs modulate the responsiveness of MEPM cells to retinoic acid. Inhibition of endogenous CRABP expression renders MEPM cells less responsive to RA with respect to induction of TGF-β3, RAR-β, and tenascin gene expression. These results have important implications for our understanding of the role of the CRABPs in retinoid teratology.

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