AKR1B3 mRNA is expressed in preadipocytes, and its level increases about 4fold at day 1 after initiation of adipocyte differentiation, and then quickly decreases the following day to a level lower than that in the preadipocytes
AKR1C3 is overexpressed in skin squamous cell carcinoma (SCC) and affects SCC growth via prostaglandin metabolism. It is upregulated by its substrate, prostaglandin D2
expression is significantly up-regulated by oestradiol plus progesterone at oestrus and the mid phase of pseudopregnancy and is also up-regulated by a single treatment with progesterone at late pseudopregnancy. Simultaneous incubation with oestradiol and progesterone up-regulates prostaglandin-endoperoxide synthase PTGS2 gene expression at oestrus and mid-luteal phase. Treatment with oestradiol and /or progesterone affects neither prostaglandin F2alpha secretion nor prostaglandin F2alpha synthase expression at any phase after 12 h of culture
expression of AKR1B1 is upregulated in the fetal membranes in association with term labor, during labor tumor necrosis factor TNF upregulates the AKR1B1 protein expression
flutamide, i.e. 2-methyl-N-[4-nitro-30-(trifluoromethyl)-phenyl]propamide, causes upregulation of enzyme PGFS mRNA and protein amount in pregnant female pigs at gestation days 90 and 108, whereas PTGF receptor protein expression is greater in both gestational periods
in cultured myometrial cells there is a dose-dependent stimulatory effect of interleukin 1beta and tumor necrosis factor alpha on PTGS2, PTGES and AKR1B1, i.e.PGF synthase expression
interleukin IL-1beta is able to upregulate COX-2 and AKR1B1 proteins as well as prostaglandin F2alpha production under normal glucose concentrations. The promoter activity of AKR1B1 gene is increased by IL-1beta particularly around the multiple stress response region
treatment with estradiol and/or progesterone affects neither PGF2alpha secretion nor enzyme PGFS expression at any phase after 12 h of culture, while related enzymes PG-endoperoxide synthase (PTGS2) and PGE2 synthase (PGES) are both upregulated by estradiol and progesterone during pseudopregnancy
flutamide, i.e. 2-methyl-N-[4-nitro-30-(trifluoromethyl)-phenyl]propamide, causes upregulation of enzyme PGFS mRNA and protein amount in pregnant female pigs at gestation days 90 and 108, whereas PTGF receptor protein expression is greater in both gestational periods
flutamide, i.e. 2-methyl-N-[4-nitro-30-(trifluoromethyl)-phenyl]propamide, causes upregulation of enzyme PGFS mRNA and protein amount in pregnant female pigs at gestation days 90 and 108, whereas PTGF receptor protein expression is greater in both gestational periods