Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present studies were designed to examine the regulation of leptin release in primary cultures of adipocytes from fed hypothyroid rats incubated with hormones for 24 hours. Leptin release was increased in the presence of dexamethasone, while the decrease in leptin mRNA content over a 24-hour incubation was reduced by dexamethasone. Dexamethasone did not affect the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA or 18S RNA content of adipocytes. Insulin increased leptin release by adipocytes in both the absence and presence of dexamethasone. Although insulin also prevented the loss of leptin mRNA, this effect was less than that observed for GAPDH mRNA or 18S RNA content. In isolated adipocytes, the loss of almost half the 18S RNA content over a 24-hour incubation was prevented in the presence of insulin but not oxytocin or epidermal growth factor (EGF). The specific beta3 catecholamine agonist CI 316,243 inhibited the effects of dexamethasone on leptin release and leptin mRNA accumulation, as did EGF, without affecting 18S RNA content. Oxytocin inhibited the increase in leptin release due to dexamethasone without affecting leptin mRNA levels. These data indicate that although dexamethasone and insulin are positive regulators of leptin release, only dexamethasone specifically prevented the loss of leptin mRNA in cultured rat adipocytes. In contrast, insulin, but not dexamethasone, prevented the marked loss in 18S RNA observed over a 24-hour incubation of rat adipocytes.
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PMID:Hormonal regulation of 18S RNA, leptin mRNA, and leptin release in adipocytes from hypothyroid rats. 986 73

A positive-feedback loop between luteal oxytocin and uterine prostaglandin F2 alpha (PGF) is a major signal for luteolysis in ruminants. Likewise, uterine PGF causes luteolysis in mares, but the involvement of oxytocin in this process is unclear. We wanted: 1) to determine if the oxytocin-neurophysin I (OT-NP I) gene is transcribed into mRNA in the endometrium of mares; and, if so, 2) to analyze relative changes in abundance of endometrial OT-NP I mRNA throughout the estrous cycle and during early stages of pregnancy. Endometrial biopsies were obtained from nonbred mares during estrus, and 5, 10, and 15 d after ovulation (n = 3/d). Biopsies were also obtained from pregnant mares 10, 15, and 20 d after ovulation (n = 3/d). Relative amounts of OT-NP I and glyceraldehyde-3-phosphate dehydrogenase mRNA in endometrium were assessed by reverse transcription-polymerase chain reaction and Southern blotting. Endometrial OT-NP I mRNA abundance changed with day of the cycle or pregnancy, and levels at estrus were higher than at any other days examined. The OT-NP I mRNA levels were negatively correlated with serum progesterone across all days examined and positively correlated with serum estradiol in nonbred mares. The reverse transcription-polymerase chain reaction products for both OT-NP I and glyceraldehyde-3-phosphate dehydrogenase were cloned into vectors and sequenced. Each shared greater than 89% nucleotide and predicted amino acid identities with the respective human, bovine, ovine, and rat products. Uterine oxytocin may be involved in regulation of reproductive tract function during the estrous cycle and/or establishment of pregnancy in horses.
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PMID:Oxytocin-neurophysin I mRNA abundance in equine uterine endometrium. 1034 20