Downregulation of long-form prolactin receptor mRNA during prolactin-induced luteal regression

Objective: Prolactin is capable of both trophic and lytic actions in rat co rpora lutea. In corpora lutea responding to a trophic prolactin signal, the long form of the prolactin receptor is the dominant form and is upregulate d by prolactin. We investigated whether mRNA for the short form of the prol actin receptor was dominant in corpora lutea responding to a lytic prolacti n signal, and whether the relative concentrations of the mRNAs for both for ms of the prolactin receptor were changed during this response, Design and methods: Immature rats were ovulated by injection of 5 IU equine chorionic gonadotrophin and 5 IU human chorionic gonadotrophin, and were h ypophysectomized shortly after ovulation. Nine days after hppophysectomy, r ats were injected with prolactin (500 mu g/day) or vehicle for 24 (n = 6, n = 6) or 72 h (n = 13, n = 5). Total RNA was isolated from corpora lutea an d mRNA for both types of prolactin receptor were analyzed by semiquantitati ve RT-PCR using the ribosomal protein S16 as the internal control. Results: The intensities of the long- and short-fe rm prolactin receptor si gnals were normalized to the S16 internal control and expressed as relative densitometric units. The normalized values at 24 h for prolactin-treated v s vehicle-treated rats were 0.23 +/- 0.05 vs 0.49 +/- 0.15 (P > 0.05) for t he short form and 4.04 +/- 0.8 vs 4.23 +/- 0.6 (P > 0.05) for the long form . The values for 72 h were 0.30 +/- 0.05 vs 0.24 +/- 0.05 (P > 0.05) for th e short form and 2.7 6 +/- 0.4 os 5.53 +/- 0.3 (P < 0.01) for the long form respectively. Conclusion: The long form of the prolactin receptor is the dominant form at both time-points; however, the concentration of mRNA for this receptor sof orm was specifically downregulated by prolactin treatment, Our results sugg est that the short form of the prolactin receptor alone is unlikely to medi ate the luteolytic action of prolactin, but that luteolytic events may be i nfluenced via a change in the ratio of the two receptor isoforms.