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Published on: January 10, 2015
Cigarette smoke inhibits endometrial epithelial cell proliferation through a nitric oxide-mediated pathway
Omid Khorram1, Guang Han, Thomas Magee
1Department of Obstetrics and Gynecology, Harbor-UCLA Medical Center, Torrance, California, USA. okhorram@obgyn.humc.edu
Objective:
To determine the direct effects of cigarette smoke (CS) on human endometrial surface epithelial cell line proliferation.
Design:
In vitro study using HES cells and primary human endometrial cells.
Setting:
University-based academic center.
Patient(S):
Premenopausal women in the proliferative phase of the cycle.
Intervention(S):
The HES cells and primary human endometrial cells were exposed to cigarette smoke-saturated solution.
Main Outcome Measure(S):
Cell proliferation and expression of different isoforms of nitric oxide synthase.
Result(S):
Cigarette smoke inhibited HES cell proliferation in a dose- and time-dependant manner. The inhibitory effect of CS was blocked by hemoglobin and enhanced by L-arginine (L-Arg). Cigarette smoking and nicotine stimulated the expression of endothelial NO synthase (eNOS) and inducible NO synthase (iNOS) whereas benzo[a]pyrene (BP) only stimulated the expression of eNOS in HES cells. Cigarette smoke stimulated the expression of eNOS/iNOS in primary human endometrial cells, comprised of epithelial and stromal cells. The effect of CS on eNOS/iNOS expression in HES cells was blocked by ascorbic acid but not by glutathione.
Conclusion(S):
Cigarette smoke inhibits endometrial cell proliferation through a nitric oxide-mediated pathway.
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