Abnormal proliferation of airway smooth muscle may contribute to the pathogenesis of obstructive airway disease. Little information is known however, ahoul factors which may serve a regulatory function to inhibit airway smooth muscle growth. We have examined the ability of the nitric oxide (NO) donor S-nitroso-N-acetylpenicillamine (SNAP) to inhibit human airway smooth muscle growth. Airway smooth muscle cells were isolated from human extrapulmonary bronchi and grown in culture for up to 3 passages in media containing 1TO fetal calf serum (PCS). Cells were plated on 24 well plates and grown in culture media until they were confluent (5-7 days). The cells were then growth arrested for 24 h in media without FCS. Cells were then exposed to media containing 10% FCS in the absence or presence of SNAP (0.03-1 mM). After 18 h, 0.5 |aCi of [methyl-3H]-ihymidine was added and 12 h later the cells were washed repeatedly and the cells soluhilid in NaOH and the amount of radioactivity counted. 10% FCS was found to produce a 13+.1 told increase in thymidine incorporation compared to cells exposed to media without FCS (n=6). This increase in thymidine incorporation was concentration dependently inhibited by SNAP. In the presence of 0.03 mM SNAP the increase produced by 10% FCS was <)3±1<X of that induced by Wfr FCS alone, in the presence of 0.1 mM, 70±6<7<, in the presence of 0.3 mM, 17+3 %, and in the presence of 1 mM, 6+1% (n=6). SNAP was also found to inhibit the increase in cell numbers and total protein content elicited by 10% FCS. These results suggest that NO may have ami-proliferative effects on human airway smooth muscle.
|Publication status||Published - Jan 1 1996|
ASJC Scopus subject areas
- Molecular Biology