|Back Topic Categories Search Previous Abstract Next Abstract|
J.L. Környei1 *, Zs. Vértes1 *, A. Oszter1 , K.A. Kovács2 , M. Vértes1
Institute of Physiology, University Medical School of Pecs, Pecs, Hungary 1
Department of Obstetrics and Gynecology, University Medical School of Pecs, Hungary 2
The effect of opioid peptides on the epidermal growth factor-induced cell proliferation in adult rat uterine primary cell-cultures was studied. Tissue specimens were dispersed by trypsin-collagenase digestions and cultured in Dulbecco's modified Eagle's medium containing 10% FBS. Treatments were present continously in the medium being changed by 48 hours. The cell densities of subconfluent cultures were detected by counting the cells after trypsinization and/or DNA content of the flasks were measured. Rat uterine primary cell-cultures reached confluency in 12-14 days showing 12.000 cells/cm2 density. Average population doubling time was about 2 days. Epidermal growth factor (EGF) increased cell densities by 60-100%. This EGF-induced stimulation of cell proliferation was decreased to control values by D-met2-pro5-enkefalinamide (ENK). This inhibition appeared after a 2-3-day latency period and was significant between 5-11 days of culture. The maximal stimulatory effect of EGF was found to be 1 nM. ENK was able to inhibit cell proliferation at each EGF concentration examined. The half effective inhibitory concentration of ENK was 1.2 nM. ENK did not have any effect on the basal proliferation rate of the adult rat uterine cells. The opioid-induced inhibition of uterine cell proliferation was blocked completely by the opiate receptor antagonist naloxone, while naloxone did not have any effect on its own. The inhibitory effect of opioid peptides was mediated by the mu opiate receptor dominantly. This inhibitory effect of EOPs was eliminated by the presence of the progesterone receptor antagonist RU486. In summary, here we present a novel physiological direct crosstalk between the opioid, epidermal growth factor and sexual steroid signaling systems having a role in the regulation of normal uterine growth. (Supported by the OTKA-T-16316 grant, Hungary)
This abstract is being presented on Monday, August 2 at 8:00 AM to 10:15 AM at CUB 2nd Floor Ballroom.