Rat Prostaglandin D₂ Synthetase: Its Tissue Distribution, Changes during Maturation, and Regulation in the Testis and Epididymis¹

^a The Population Council, New York, New York 10021 ^b Institute of Pharmacology and Pharmacognosy, University of Rome "La Sapienza", Rome, Italy

The changes in glutathione-independent prostaglandin D₂ synthetase (PGD-S) during maturation in the rat were determined in selected organs by an RIA using PGD-S purified from rat cerebrospinal fluid and a monospecific anti-rat PGD-S polyclonal antibody. In a survey of its tissue distribution in various organ extracts and biological fluids, it was found that the concentration of PGD-S was highest in the epididymis—about 6- and 80-fold greater than that in the brain and testis, respectively. During maturation, PGD-S concentration increased steadily in the testis and epididymis; this is in contrast to the pattern of changes in the brain and liver, which showed a general trend of decline. Reverse transcription-polymerase chain reaction and Southern blotting were used to demonstrate the presence of PGD-S mRNA transcript in the testis and in Sertoli and germ cells. In the epididymis, the steady-state PGD-S mRNA level was highest in the caput, followed by the cauda and corpus. Orchiectomy induced a drastic reduction of PGD-S concentration in all three epididymal compartments. Administration of dihydrotestosterone (DHT) failed to restore the reduced epididymal PGD-S level except in the caput epididymis, where 4 days after DHT treatment the level of PGD-S was restored to about 50% of the pre-orchiectomized level; this suggests that the epididymal PGD-S level is not entirely regulated by androgen and that another yet to be identified testicular factor(s) is likely to be involved in its regulation. Germ cell-conditioned medium was also shown to stimulate PGD-S expression in the Sertoli cell. These results illustrate that PGD-S is an important molecule in testicular and epididymal function and that it is likely involved in spermatogenesis and sperm maturation.

¹ Supported in part by grants from the Sovena Foundation, the Noopolis Foundation, the Rockefeller Foundation (PS9601, PS9721), the CONRAD Program (CIG-96–05), and NIH (HD-13541).

² Correspondence: C. Yan Cheng, The Population Council, 1230 York Avenue, New York, NY 10021. FAX: (212) 327–7678; yan{at}popcbr.rockefeller.edu

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