Abstract:
BACKGROUND:Cyclooxygenase (COX)-2 contributes to vascular smooth muscle cell (VSMC) proliferation induced by tumor necrosis factor (TNF) and angiotensin II. The present study demonstrates, however, that depending on prevailing conditions, COX-2-derived prostanoids may also inhibit VSMC proliferation. METHODS AND RESULTS:TNF-alpha stimulated proliferation of VSMCs by shortening the G1 phase of the cell cycle. This effect was abolished by NS-398, a selective COX-2 inhibitor. Addition of TNF did not affect the protein-to-DNA ratio, measured by flow cytometry, suggesting that TNF does not induce VSMC hypertrophy. Inhibition of nitric oxide synthase (NOS) activity attenuated TNF-mediated increases in prostaglandin (PG) I2 synthesis, whereas thromboxane (TX) A2 production and COX-2 protein expression were unaffected. Moreover, inhibition of NOS activity increased TNF-mediated proliferation by approximately 23%. Thus, NO preferentially stimulates PGI2 production, suggesting that production of NO by VSMCs challenged with TNF limits the ability of the cytokine to increase proliferation. NO donors increased COX-2 protein expression and PGI2 synthesis, had no effect on TXA2 production, and decreased cell numbers by 50%, indicating that expression of COX-2 per se might not be sufficient to support proliferation. The effects of NO donors were prevented when COX-2 activity was inhibited with NS-398. CONCLUSIONS:The COX-2-dependent proliferative response of VSMCs to TNF was modulated in an NO-dependent manner, and PGI2 derived from COX-2 might contribute to the antiproliferative effect of NO donors.
journal_name
Circulationjournal_title
Circulationauthors
Haider A,Lee I,Grabarek J,Darzynkiewicz Z,Ferreri NRdoi
10.1161/01.CIR.0000085211.97972.2Csubject
Has Abstractpub_date
2003-08-26 00:00:00pages
1015-21issue
8eissn
0009-7322issn
1524-4539pii
01.CIR.0000085211.97972.2Cjournal_volume
108pub_type
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