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This version published online on December 22, 2003
Endocrinology, doi:10.1210/en.2003-0742
A more recent version of this article appeared on April 1, 2004
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Submitted on June 12, 2003
Accepted on December 15, 2003

Disparate Effects of Thyroid Hormone on Actions of EGF and TGF-{alpha} Are Mediated by Cyclic-AMP-Dependent Protein Kinase II

Ai Shih1, Shenli Zhang1, H. James Cao1, Heng-Yuan Tang1, Faith B. Davis1*, Paul J. Davis1, and Hung-Yun Lin1

1 Research Service, Stratton Veterans Affairs Medical Center, the Ordway Research Institute, Inc. and the Wadsworth Center, New York State Department of Health, Albany, NY 12208

* To whom correspondence should be addressed. E-mail: pjdavis{at}albany.net.

Epidermal growth factor (EGF) and transforming growth factor-{alpha} (TGF-{alpha}) share the same plasma membrane receptor (EGFR). In the present studies in HeLa cells, both EGF and TGF-{alpha} caused mitogen-activated protein kinase (MAPK; ERK1/2) activation and expression of the immediate-early gene c-fos. Thyroid hormone (L-thyroxine, T4) nongenomically enhanced EGF- and TGF-{alpha}-induced MAPK activation. This T4 action was duplicated by T4-agarose and blocked by tetraiodothyroacetic acid which inhibits binding of T4 to plasma membranes. TGF-{alpha}-induced MAPK activation was potentiated by 8-Br-cAMP, but not by 8-Cl-cAMP. TGF-{alpha}, T4 and 8-Br-cAMP each caused PKA-II serine phosphorylation, whereas phosphorylation of PKA-II was not seen in cells treated with EGF or 8-Cl-cAMP. In a PKA activity assay, the enzyme was stimulated by T4, EGF and TGF-{alpha}; T4 enhanced the effect of TGF-{alpha}, but not that of EGF. T4, while it potentiated c-fos gene expression in EGF-treated cells, suppressed this effect in cells treated with TGF-{alpha}. Cells exposed to 8-Br-cAMP also inhibited TGF-{alpha}-stimulated c-fos expression. Studies of cell proliferation indicated that T4 potentiated EGF action but inhibited that effect in TGF-{alpha}-treated cells. The disparate effects of T4 on actions of EGF and TGF-{alpha}, which share the same cell surface receptor, are mediated by hormone phosphorylation and activation of PKA-II.




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