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Anti-mitogenic action of opioid peptides on epidermal growth factor-stimulated uterine cells
J L Környei1, A Oszter, K A Kovács
1Institute of Physiology, Pécs University, Medical School, Szigeti str. 12, Pécs H-7643, Hungary. Jozsef.Kornyei@aok.pte.hu
Abstract:
Endogenous opioid peptides are negative regulators of estradiol-induced uterine cell proliferation. To investigate the possible molecular target site(s) of their anti-mitogenic action, we examined the effect of opioid peptides on epidermal growth factor-induced cell proliferation both in uterine primary cell cultures prepared from adult rats and in human myometrial smooth muscle cell lines. Epidermal growth factor (EGF) significantly increased cell density in both types of cultured monolayers. This EGF-induced stimulation of cell proliferation was blocked by [D-Met(2)-Pro(5)]enkephalinamide in a time-dependent, receptor-mediated manner. The effective concentrations were within the physiological nanomolar range. Enkephalinamide did not have any effect on the basal rate of proliferation of the uterine cells. Our results on this novel physiological cross-talk suggest that shared step(s) of the mechanism of action of estradiol and EGF might be targeted by opioid peptides and not the general machinery of cell proliferation.
Insights
Opioid peptides inhibit uterine cell growth stimulated by epidermal growth factor (EGF). This suggests opioid peptides target shared pathways of estradiol and EGF, not general cell proliferation machinery.
Area of Science:
- Reproductive biology
- Endocrinology
- Cell signaling
Background:
- Endogenous opioid peptides regulate estradiol-induced uterine cell proliferation.
- The molecular targets of opioid peptide anti-mitogenic action require elucidation.
Purpose of the Study:
- To investigate the effect of opioid peptides on epidermal growth factor (EGF)-induced uterine cell proliferation.
- To determine if opioid peptides target shared signaling pathways with estradiol or general proliferation mechanisms.
Main Methods:
- Primary rat uterine cell cultures and human myometrial smooth muscle cell lines were used.
- Cells were treated with EGF to stimulate proliferation.
- The effect of [D-Met(2)-Pro(5)]enkephalinamide on EGF-induced proliferation was assessed.
Main Results:
- Epidermal growth factor (EGF) significantly increased uterine cell density in both rat and human cell models.
- [D-Met(2)-Pro(5)]enkephalinamide blocked EGF-induced proliferation in a time-dependent, receptor-mediated manner at physiological concentrations.
- Opioid peptides did not affect basal uterine cell proliferation rates.
Conclusions:
- Opioid peptides act as negative regulators of EGF-induced uterine cell proliferation.
- Results suggest opioid peptides target shared molecular steps in estradiol and EGF signaling pathways.
- This cross-talk indicates a specific mechanism rather than a general effect on cell proliferation machinery.
