Abstract:
:1. Oestrogen reduces vascular smooth muscle cell proliferation in mouse vascular injury models. Data on the antiproliferative effect of oestrogen in cultured vascular smooth muscle cells (VSMC) are less conclusive than those obtained in whole animal studies. 2. In the present study, we investigated the hypothesis that oestrogen-induced attenuation of VSMC proliferation is facilitated by the presence of endothelial cells (EC) using a coculture system of EC and VSMC. 3. Treatment with a physiological concentration of oestrogen (17beta-estradiol (E2); 100 nmol/L) had no effect on fetal calf serum (FCS)-stimulated DNA synthesis in either A7r5 VSMC or bEnd.3 EC. However, stimulation of bEnd. 3 cells with E2 in a coculture system of bEnd.3 and A7r5 cells reduced FCS-induced DNA synthesis in A7r5 cells by approximately 45%. The nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (l-NAME; 100 micromol/L) did not reverse the oestrogen-induced attenuation of DNA synthesis. The antiproliferative effect of E2 may be mediated via either oestrogen receptor (ER) alpha, ERbeta or both because the bEnd.3 cells expressed immunoreactivity for both ER subtypes. 4. These data show that ERalpha- and ERbeta-expressing endothelial cells, which are stimulated with a physiological concentration of oestrogen, release a factor(s) that arrests the proliferation of cocultured VSMC. Oestrogen-induced attenuation of vascular smooth muscle cell proliferation is not prevented by L-NAME, suggesting that a mechanism other than endothelial NO is involved.
journal_name
Clin Exp Pharmacol Physioljournal_title
Clinical and experimental pharmacology & physiologyauthors
Odenlund M,Ekblad E,Nilsson BOdoi
10.1111/j.1440-1681.2007.04870.xsubject
Has Abstractpub_date
2008-03-01 00:00:00pages
245-8issue
3eissn
0305-1870issn
1440-1681pii
CEP4870journal_volume
35pub_type
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