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Progesterone Is a Suppressor of Apoptosis in Bovine Luteal Cells¹

Laboratory of Reproductive Endocrinology,³Department of Animal Science, Faculty of Agriculture, Okayama University, Okayama 700-8530, Japan Division of Reproductive Endocrinology and Pathophysiology,⁴ Institute of Animal Reproduction and Food Research, PAS, Olsztyn 10-747, Poland

Progesterone is suggested to be a suppressor of apoptosis in bovine luteal cells. Fas antigen (Fas) is a cell surface receptor that triggers apoptosis in sensitive cells. Furthermore, apoptosis is known to be controlled by the bcl-2 gene/protein family and caspases. This study was undertaken to determine whether intraluteal progesterone (P4) is involved in Fas L–mediated luteal cell death in the bovine corpus luteum (CL) in vitro. Moreover, we studied whether an antagonist of P4 influences gene expression of the bcl-2 family and caspase-3 and the activity of caspase-3 in the bovine CL. Luteal cells obtained from the cows in the midluteal phase of the estrous cycle (Days 8–12 of the cycle) were exposed to a specific P4 antagonist (onapristone [OP], 10^–4 M) with or without 100 ng/ml Fas L. Although Fas L alone did not show a cytotoxic effect, treatment of the cells with OP alone or in combination with Fas L resulted in killing of 30% and 45% of the cells, respectively (P < 0.05). DNA fragmentation was observed in the cells treated with Fas L in the presence of OP. The inhibition of P4 action by OP increased the expression of Fas mRNA (P < 0.01); however, it did not affect bax or bcl-2 mRNA expression (P > 0.05). Moreover, OP stimulated expression of caspase-3 mRNA (P < 0.01). The overall results indirectly show that intraluteal P4 suppresses apoptosis in bovine luteal cells through the inhibition of Fas and caspase-3 mRNA expression and inhibition of caspase-3 activation.

¹ Supported by Grants-in-Aid for Scientific Research from the Japan Society for the Promotion of Science (JSPS: (B)14360168), Polish Ministry of Scientific Research and Information Technology (PBZ-KBN-084/P06/2002/ 5.2), and Japanese-Polish Joint Research Project under the agreement between JSPS and the Polish Academy of Sciences (PAS).

² Correspondence: FAX: +81 86 251 8388; kokuda{at}cc.okayama-u.ac.jp

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