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Cardiovascular Research 2003 59(3):734-744; doi:10.1016/S0008-6363(03)00496-6
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Estrogen receptor β mediates the inhibitory effect of estradiol on vascular smooth muscle cell proliferation

Tokumitsu Watanabea, Masahiro Akishitab, Takashi Nakaokac, Koichi Kozakia, Yukiko Miyaharaa, Hong Hea, Yumiko Ohikea, Teruhiko Ogitad, Satoshi Inouea, Masami Muramatsue, Naohide Yamashitac and Yasuyoshi Ouchia,*

aDepartment of Geriatric Medicine, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
bDepartment of Geriatric Medicine, Kyorin University School of Medicine, Tokyo 181-8611, Japan
cDepartment of Advanced Medicine, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan
dDepartment of Cardiovascular Medicine, University of Tokyo, Tokyo 113-8655, Japan
eResearch Center for Genomic Medicine, Saitama Medical School, Saitama 350-1241, Japan

youchi-tky{at}umin.ac.jp

* Corresponding author. Tel.: +81-3-5800-8830; fax: +81-3-5800-6530.

Objectives: It has been demonstrated that 17β-estradiol (E2) has an inhibitory effect on the proliferation of vascular smooth muscle cells (VSMCs) through an estrogen receptor (ER)-dependent pathway. Both ER subtypes, classical ER (ER{alpha}) and the newly identified ER subtype (ERβ), are expressed in VSMCs. However, it remains unknown which receptor plays the critical role in the inhibitory effect on VSMC proliferation. Methods and results: We constructed replication-deficient adenoviruses bearing the coding region of human ER{alpha}, ERβ, and the dominant-negative form of ERβ (designated AxCAER{alpha}, AxCAERβ, and AxCADNERβ, respectively). Prior to infection with the adenoviruses, 100 nmol/l E2 attenuated DNA synthesis by up to 14% and transactivated the estrogen-induced expression of the desired mRNA in rat VSMCs. This was accompanied by increased transcriptional activity of estrogen responsive element in response to E2, and the increase was comparable between AxCAER{alpha} and AxCAERβ. When VSMCs were infected with AxCAERβ at a multiplicity of infection of 5 or higher, DNA synthesis as well as cell number decreased by 50% in response to E2, and the effect was abolished by co-infection with AxCADNERβ. In contrast, when VSMCs were infected with AxCAER{alpha}, the reduction in DNA synthesis was minimal. Conclusions: Our results indicate that ERβ is more potent than ER{alpha} in the inhibitory effect on VSMC proliferation.

KEYWORDS Atherosclerosis; Gene expression; Hormones; Receptors; Smooth muscle


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