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M205616200v1
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Papers In Press, published online ahead of print November 21, 2002
J. Biol. Chem, 10.1074/jbc.M205616200
Submitted on June 6, 2002
Revised on November 6, 2002
Accepted on November 20, 2002

Endothelin-1 specific activation of B-type natriuretic peptide gene via p38 mitogen activated protein kinase and nuclear ETS factors

Sampsa Pikkarainen, Heikki Tokola, Risto Kerkelä, Theresa Majalahti-Palviainen, Olli Vuolteenaho, and Heikki Ruskoaho

Pharmacology and Toxicology, Biocenter Oulu, University of Oulu, Oulu

Corresponding Author: heikki.ruskoaho{at}oulu.fi

Terminally differentiated cardiac myocytes adapt to mechanical and neurohumoral stress via morphological changes of individual cells accompanied by reactivation of fetal pattern of gene expression. Endothelin-1, a powerful paracrine mediator of myocyte growth, induces similar changes in cultured cardiac myocytes as those seen in hypertrophied heart in vivo. By using of rat B-type natriuretic peptide promoter, we identified a novel ETS binding sequence, on which nuclear protein binding is activated in endothelin-1 treated cultured cardiac myocytes. This sequence binds ETS-like gene-1 transcription factor and mediates endothelin-1-specific activation of transcription, but not responses to increased calcium signaling via L-type calcium channels, angiotensin II treatment or mechanical stretch of myocytes. Interestingly, endothelin-1 activated signaling converges via p38 mitogen activated protein kinase dependent mechanism on ETS binding site, whereas this element inhibits extracellular signal-regulated kinase activated transcription. In conclusion, given the fundamental role of the interaction of mitogen activated protein kinases and ETS factors in regulation of eukaryotic cell differentiation, growth and oncogenesis, these results provide the unique evidence of a endothelin-1 and mitogen activated protein kinase regulated ETS factor pathway for cardiac myocytes.


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