Abstract: 403

PRL AND TGF1 PLAY OPPOSITE ROLES IN THE REGULATION OF APOPTOSIS IN THE RAT DECIDUA.

Christian Tessier^{1 *}, Anne Prigent-Tessier^{1 *}, Susan Ferguson-Gottschall¹ , Geula Gibori^{1 *}
Dept of Physiology and Biophysics University of Illinois at Chicago Chicago IL ¹

TGF1 belongs to a large family of cytokines that exert a wide range of biological effects including cell growth regulation and apoptosis. In rat decidua, extensive apoptosis takes place during pregnancy to accommodate the developing conceptus and coincides with TGF1 mRNA expression. Thus, we examined whether TGF1 plays a role in apoptosis. Primary decidual cells were collected from day 9 pseudopregnant rats and treated with TGF1 for 72 hrs. The addition of TGF1 stimulated DNA fragmentation in a dose-dependent manner. Since TGF1 has been shown to inhibit PRL which is known to have anti-apoptotic effect, and since we have recently shown that rat decidua produces and secretes PRL, we examined whether TGF1 can affect PRL expression. Primary decidual cells were cultured in the presence of TGF1 for 12 hrs. The results showed that TGF1 caused a down-regulation of PRL mRNA expression. Because the PRL receptor disappears from the decidua at a time when this tissue undergoes extensive apoptosis, we then examined whether PRL can prevent apoptosis. Primary decidual cells obtained from day 9 of pseudopregnancy were transfected with either the long or the short form of the PRL receptor (PRL-RL or PRL-RS respectively) or both. The results revealed that PRL decreased DNA laddering only in cells transfected with either the PRL-RL or both PRL-RL and PRL-RS. In summary, this study demonstrates that TGF1 and PRL play opposite roles in the regulation of apoptosis in rat decidua. By decreasing PRL expression, TGF1 may induce the apoptotic process in the decidua. The results also show for the first time that PRL, via the PRL-RL, can prevent apoptosis in decidua suggesting a crucial role for this hormone in the maintenance of pregnancy. Supported by NIH HD-12356 (GG) and Ernst Schering Research Foundation (CT).

    This abstract is being presented on Monday, August 2 at 1:30 PM at Todd 125.