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Flutamide Influences Placental Aldo–Keto Reductase Family 1 Member C 1 ( AKR 1 C 1) Expression in Pigs
Author(s) -
Grzesiak M,
KnapczykStwora K,
Wieciech I,
Golas A,
Slomczynska M
Publication year - 2014
Publication title -
reproduction in domestic animals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.546
H-Index - 66
eISSN - 1439-0531
pISSN - 0936-6768
DOI - 10.1111/rda.12263
Subject(s) - flutamide , placenta , gestation , biology , endocrinology , medicine , andrology , androgen , stromal cell , androgen receptor , messenger rna , fetus , pregnancy , hormone , cancer , gene , prostate cancer , biochemistry , genetics
Contents Aldo–keto reductase family 1 member C 1 ( AKR 1 C 1) catalyses the conversion of progesterone into inactive 20 α ‐dihydroxyprogesterone. It is suggested that AKR 1 C 1 expression in the placenta prevents from the cytotoxic effect of progesterone on foetuses during late pregnancy. The aim of the study was to determine whether the anti‐androgen flutamide administered during late pregnancy (83–89 days of gestation) or before parturition (101–107 days of gestation) influences AKR 1 C 1 expression in the porcine placenta. AKR 1 C 1 mRNA and protein levels were measured using real‐time PCR and western blotting, respectively. Immunolocalization of AKR 1 C 1 within placentas was also performed. Flutamide significantly increased AKR 1 C 1 mRNA (p = 0.008) and protein (p = 0.019) expression only during the pre‐parturient period in pigs. AKR 1 C 1 protein was immunolocalized in the epithelial and stromal cells of foetal and maternal part of placenta at both stages of gestation. Following flutamide treatment, the intensity of staining was higher (p = 0.045) on day 108 of gestation. In conclusion, porcine placental AKR 1 C 1 expression seems to be regulated by an androgen signalling pathway and may be involved in foetal survival by preventing the detrimental effect of progesterone.