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Volume 272, Number 21, Issue of May 23, 1997 pp. 13711-13716
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

All-trans-retinoic Acid Increases Transforming Growth Factor-2 and Insulin-like Growth Factor Binding Protein-3 Expression through a Retinoic Acid Receptor--dependent Signaling Pathway

(Received for publication, December 24, 1996, and in revised form, February 19, 1997)

Gil-Ro Han , David F. Dohi , Ho-Young Lee , Roopmathy Rajah ^§ , Garrett L. Walsh ^¶ , Waun Ki Hong , Pinchas Cohen ^§ and Jonathan M. Kurie

From the Departments of  Thoracic/Head and Neck Medical Oncology and ^¶ Thoracic and Cardiovascular Surgery, University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030 and the ^§ Department of Pediatrics, University of Pennsylvania, Philadelphia, Pennsylvania 19104

Retinoids, including retinol and retinoic acid derivatives, maintain the normal growth and differentiation of human bronchial epithelial cells. The signaling pathways through which retinoids mediate these effects have not been defined. Insulin-like growth factor binding protein-3 (IGFBP-3) and the transforming growth factor- (TGF-) gene family (1-3) were examined as potential components of the retinoid signaling pathway in normal human bronchial epithelial cells. All-trans-retinoic acid (t-RA) increased the levels of TGF-2 and IGFBP-3 mRNA and of secreted TGF- and IGFBP-3 proteins. An antagonist of retinoic acid receptor-, LG100629, abrogated the increase in TGF-2 and IGFBP-3 mRNA levels induced by t-RA. t-RA increased IGFBP-3 mRNA levels transiently from 1 to 6 h, and subsequently a sustained increase began at 72 h, which coincided with the appearance of active TGF- in the media. Treatment with TGF-2 increased IGFBP-3 mRNA levels, but treatment with latency-associated peptide, which inactivates secreted TGF-, did not abrogate the effect of t-RA on IGFBP-3 expression. These findings provide evidence that t-RA increased TGF-2 and IGFBP-3 expression through an retinoic acid receptor--dependent pathway, and the increase in IGFBP-3 expression by t-RA did not require activation of the TGF- pathway by autocrine or paracrine mechanisms.

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