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Constitutive Expression of Prostaglandin-Endoperoxide Synthase 2 by Somatic and Spermatogenic Cells Is Responsible for Prostaglandin E₂ Production in the Adult Rat Testis¹

Monash Institute of Medical Research,⁴ and Department of Physiology,⁵ Monash University, Clayton, Victoria 3168, Australia

ABSTRACT

Prostaglandins (PGs), particularly PGE₂, have been implicated in the control of testicular steroidogenesis, spermatogenesis, and local immunity. However, virtually nothing is known about the expression or activity of the prostaglandin-endoperoxide synthases (PTGSs; also referred to as the cyclooxygenases), the specific rate-limiting enzymes responsible for PG production, in the adult testis. This activity was investigated in rats under normal conditions and during lipopolysaccharide-induced inflammation using quantitative real-time PCR, in situ hybridization, Western blotting, and PGE₂ measurements by ELISA. The mRNA for both the "constitutive" Ptgs1 and the "inducible" Ptgs2 forms was detected in multiple testicular cell types. Testicular Ptgs2 expression was substantially higher than that of Ptgs1, and testicular production of PGE₂ in vitro was found to be suppressed by a specific PTGS2 inhibitor (NS-398), but not by an inhibitor of PTGS1. Further investigation indicated that 1) PGE₂ production in the adult testis is attributable to constitutive expression of PTGS2 by somatic (Leydig cells and Sertoli cells) and spermatogenic cells; 2) testicular macrophages constitutively produce relatively low levels of PTGS2 and PGE₂ but are the only cell type to respond significantly to an inflammatory stimulus by increasing production of PGE₂; and 3) testicular PTGS2 expression and intratesticular PGE₂ levels are only marginally affected by acute inflammation. These data point toward a previously unanticipated maintenance role for the "inducible" PTGS2 enzyme in normal testicular function, as well as an anomalous response of testicular PTGS2 to inflammatory stimuli. Both observations are consistent with the reduced capacity of the testis to initiate and support inflammatory reactions.

immunology, Leydig cells, male reproductive tract, Sertoli cells, testis

³Current address: School of Biomedical Sciences, University of Newcastle, Callaghan, NSW 2308, Australia.

¹Supported by a Program Grant from the National Health and Medical Research Council (NHMRC grant no. 143786), an NHMRC Project Grant (no. 194423), and by NHMRC Fellowships awarded to M.P.H. (no. 143788) and M.K.O. (no. 143781).

Correspondence: ²Wendy R. Winnall, Centre for Reproduction and Development, Monash Institute of Medical Research, 27-31 Wright St., Clayton, VIC 3168, Australia. FAX: 61 3 9594 7111; e-mail: wendy.winnall{at}med.monash.edu.au

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