[Effects of cigarette smoke extract on proliferation and ET-1 release of airway smooth muscle cells].
OBJECTIVE
To investigate whether the effect of smoking on airway smooth muscle cells (ASMC) is mediated by the autocrine action of endothelin-1 (ET-1).


METHODS
Abbit ASMC was cultured exposed to cigarette smoke extract (CSE), we examined the mitogenic effect CSE on ASMC in vitro and whether the ETA receptor antagonist JKC-301 can inhibit this effect.


RESULTS
The exposure of ASMC to 10% and 30% CSE resulted in obvious cytotoxity. The viability of ASMC was decreased, the lipid peroxides (MDA) formation was increased, and the release of lactate dehydrogenase (LDH) into supernatant was enhanced. 5% CSE significantly enhanced the cultured ASMC[3H]-thymidine (3H-TdR) incorporation by 59.9% (P < 0.01) over control. The ASMC proliferative response to 5% CSE was dose-dependently inhibited by JKC-301. Moreover, 5% CSE evoked time-dependent release of endogenous ET-1 from ASMC.


CONCLUSIONS
These data demonstrate that 5% CSE mediates ASMC proliferation via release and autocrine mitogenic action ET-1.
Fang
Q
Q
Respiratory Department, Third Teaching Hospital, Beijing Medical University.
Zhao
M
M
Ren
G
G
D000280:Administration, Inhalation; D000818:Animals; D002455:Cell Division / Q000187:drug effects; D019332:Endothelin-1 / Q000096:biosynthesis*; D008173:Lung Diseases, Obstructive / Q000209:etiology; D009130:Muscle, Smooth / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D011817:Rabbits; D012907:Smoking / Q000009:adverse effects*; D014132:Trachea / Q000187:drug effects
D019332:Endothelin-1