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This Article Full Text Full Text (PDF) All Versions of this Article: 70/1/191    most recent biolreprod.103.019083v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal My Folders Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Okuda, K. Articles by Skarzynski, D. J. Search for Related Content PubMed PubMed Citation Articles by Okuda, K. Articles by Skarzynski, D. J. Agricola Articles by Okuda, K. Articles by Skarzynski, D. J.

Interferon- Blocks the Stimulatory Effect of Tumor Necrosis Factor- on Prostaglandin F₂ Synthesis by Bovine Endometrial Stromal Cells¹

Laboratory of Reproductive Endocrinology,³ Faculty of Agriculture, Okayama University, Okayama 700-8530, Japan Department of Animal Breeding and Reproduction,⁴ National Institute of Livestock and Grassland Science, Ibaraki 305-0901, Japan Division of Reproductive Endocrinology and Pathophysiology,⁵ Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn 10-747, Poland

Tumor necrosis factor- (TNF) has been shown to be a potent stimulator of prostaglandin (PG) F₂ synthesis in bovine endometrial stromal cells. The aims of the present study were to determine the effect of interferon- (IFN) on TNF-stimulated PGF₂ synthesis and the intracellular mechanisms of TNF and IFN action in the stromal cells. When cultured bovine stromal cells were exposed to TNF (0.006–0.6 nM) for 24 h, the production of PGF₂ and cyclooxygenase (COX)-2 gene expression were stimulated by TNF (0.06–0.6 nM, P < 0.05). Moreover, a specific COX-2 inhibitor (NS-398; 5 nM) blocked the stimulatory effect of TNF on PGF₂ production (P < 0.05). Although IFN (0.03–30 ng/ml) did not stimulate basal PGF₂ production in the stromal cells, it suppressed TNF action in PGF₂ production dose dependently (P < 0.05). Moreover, the stimulatory effect of TNF (0.6 nM) on COX-2 gene expression was completely blocked by IFN (30 ng/ml; P < 0.05), although the gene expression of COX-2 was not influenced by IFN. The overall results indicate that the stimulatory effect of TNF on PGF₂ production is mediated by the up-regulation of COX-2 gene expression and suggest that one of the mechanisms of the inhibitory effect of IFN on luteolysis is the inhibition of TNF action in PGF₂ production in the stromal cells by the down-regulation of COX-2 gene expression stimulated by TNF.

¹ This research was supported by the Grants-in-Aid for Scientific Research from the Japan Society for the Promotion of Science (JSPS: (B)14360168); the Japanese Ministry of Agriculture, Forestry, and Fisheries (RCP2002-4210); and Polish State Committee for Scientific Research (KBN 5P06K 003 21), and Japanese-Polish Joint Research Project under the agreement between JSPS and the Polish Academy of Sciences.

² Correspondence: Kiyoshi Okuda, Laboratory of Reproductive Endocrinology, Faculty of Agriculture, Okayama University, Okayama 700-8530, Japan. FAX: 81 86 251 8388; kokuda{at}cc.okayama-u.ac.jp

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