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Cortisol Is a Suppressor of Apoptosis in Bovine Corpus Luteum¹

Laboratory of Reproductive Endocrinology,³ Graduate School of Natural Science and Technology, Okayama University, Okayama 700-8530, Japan Reproductive Biology Research Unit,⁴ National Institute of Agrobiological Sciences, Ibaraki 305-0901, Japan Department of Agricultural and Life Science,⁵ Obihiro University of Agriculture and Veterinary Medicine, Obihiro 080-8555, Japan Department of Reproductive Immunology,⁶ Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn 10-747, Poland

ABSTRACT

Glucocorticoid (GC) acts as a modulator of physiological functions in several organs. In the present study, we examined whether GC suppresses luteolysis in bovine corpus luteum (CL). Cortisol (an active GC) reduced the mRNA expression of caspase 8 (CASP8) and caspase 3 (CASP3) and reduced the enzymatic activity of CASP3 and cell death induced by tumor necrosis factor (TNF) and interferon gamma (IFNG) in cultured bovine luteal cells. mRNAs and proteins of GC receptor (NR3C1), 11beta-hydroxysteroid dehydrogenase type 1 (HSD11B1), and HSD11B2 were expressed in CL throughout the estrous cycle. Moreover, the protein expression and the enzymatic activity of HSD11B1 were high at the early and the midluteal stages compared to the regressed luteal stage. These results suggest that cortisol suppresses TNF-IFNG-induced apoptosis in vitro by reducing apoptosis signals via CASP8 and CASP3 in bovine CL and that the local increase in cortisol production resulting from increased HSD11B1 at the early and midluteal stages helps to maintain CL function by suppressing apoptosis of luteal cells.

apoptosis, cattle, corpus luteum, glucocorticoid, glucocorticoid receptor

¹Supported by a Grant-in-Aid for Scientific Research (No. 18380166) of the Japan Society for the Promotion of Science (JSPS). R.N. was supported by a JSPS Research Fellowship (No. 03589). H.-Y.L. is supported by a scholarship from the Ministry of Education, Culture, Sports, Science and Technology, Japan.

Correspondence: ²FAX: 81 86 251 8333; e-mail: kokuda{at}cc.okayama-u.ac.jp