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Originally published In Press as doi:10.1074/jbc.M201375200 on October 29, 2002

J. Biol. Chem., Vol. 278, Issue 1, 672-678, January 3, 2003
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alpha 1-Adrenergic Receptor Subtypes Differentially Control the Cell Cycle of Transfected CHO Cells through a cAMP-dependent Mechanism Involving p27Kip1*

Katsushi Shibata, Susumu Katsuma, Takaaki Koshimizu, Hitomi Shinoura, Akira Hirasawa, Akito Tanoue, and Gozoh TsujimotoDagger

From the Department of Molecular and Cell Pharmacology, National Center for Child Health and Development Research Institute, 3-35-31 Taishido, Setagaya-Ku, Tokyo 154-8567, Japan

Three distinct subtypes of alpha 1-adrenergic receptors (alpha 1A-, alpha 1B-, and alpha 1D-AR) play a prominent role in cell growth. However, little is known about subtype-specific effects on cell proliferation. The activation of alpha 1A- or alpha 1B-AR inhibits serum-promoted cell proliferation, whereas alpha 1D-AR activation does not show such an inhibitory effect. Notably, cell-cycle progression was blocked at G1/S transition after activation of alpha 1A/alpha 1B-AR but not of alpha 1D-AR. In agreement with the differential cell proliferation effect, cAMP production was increased after activation of alpha 1A/alpha 1B-AR but not alpha 1D-AR, whereas all alpha 1-AR subtypes are associated with inositol 1,4,5-trisphosphate production and mitogen-activated protein kinase activation in a similar fashion. Furthermore, the serum-induced reduction in the levels of the cyclin-dependent kinase inhibitor, p27Kip1, was blocked after activation of alpha 1A/alpha 1B-AR but not alpha 1D-AR. These results show that alpha 1-AR subtypes differentially activate the cAMP/p27Kip1 pathway and thereby have differential inhibitory effects on cell proliferation. Subtype-dependent effects should be taken into consideration when assessing the physiological response of native cells where alpha 1-AR subtypes are generally co-expressed.

* This work was supported in part by research grants from the Scientific Fund of the Ministry of Education, Science, and Culture of Japan; the Japan Health Science Foundation and Ministry of Human Health and Welfare; the Organization for Pharmaceutical Safety and Research; and a grant for Liberal Harmonious Research Promotion System from the Ministry of Education, Culture, Sports, Science and Technology of Japan.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger To whom correspondence should be addressed. Tel.: 81-3-3419-1252; Fax: 81-3-3419-1252; E-mail: gtsujimoto@nch.go.jp.

Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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