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5 at 0?h; 5.19%?��?0.98 vs. 13.35%?��?0.98 at 24?h; 5.48%?��?0.83 vs. 16.01%?��?0.83 at 48?h; and 1.62%?��?0.84 vs. 5.58%?��?0.84 at 96?h; P?MASP1 and non-steroidogenic cells were observed at 96?h of culture (P?PFI-2 cell line in distinct endocrine cell types has been described [21], [22], [23]?and?[24]. However, the mechanisms involved are not completely elucidated. According to Li and Johnson [25], bFGF inhibits androstenedione production in chicken granulosa cells via inhibition of P450c17�� expression. In addition, Kobayashi et?al. [21] suggest that, in bovine CL endothelial cells, the production of angiotensin II and prostaglandin F2�� are up-regulated by bFGF and VEGF and that their interactions ensure progesterone production in the developing CL. An additional study using bovine CL reported decreases in plasma P4 and STAR expression after in?vivo treatment using anti-VEGF antibody [26]. In bovine placental cells, we observed that the concentrations of P4 and E1S changed depending on the gestational age after VEGFA addition. At day 90, for example, P4 and E1S increased after treatment. At this stage, at which the placenta grows rapidly, a peak of VEGFA expression is observed [2]. In parallel, the plasma concentrations of estrogens AZD6738 cost start to rise [27], [28]?and?[29], supporting caruncular growth and differentiation [30]. In addition, progesterone levels increase once the maternal caruncle cells begin to produce substantial quantities of this hormone [31]. At day 210 in this study, the P4 and E1S concentrations were, respectively, increased and decreased in response to VEGFA addition. An increase in progesterone synthesis by the bovine placenta after day 200 of pregnancy is necessary for its maintenance because the activity of the corpus luteum declines dramatically by mid-gestation [32]. During this period, the activity of HSD3B increases ( [33]), and STAR expression and P4 synthesis increase concurrently [34], [35], [36]?and?[37]. We suggest that VEGFA can act as a local regulator of this process, most likely by modulating the expression of steroidogenic enzymes other than aromatase P450.