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)

This study was undertaken to examine the importance of nitric oxide (NO) generated by the neural isoform of the nitric oxide synthase (nNOS) on the activity of the hypothalamic neurohypophyseal system in neural nitric oxide synthase knock-out (KO) and wild-type (WT) mice under basal conditions and in response to forced swimming. The intensity of the hybridisation signal for vasopressin (AVP) in the hypothalamic supraoptic nucleus (SON) was significantly higher in KO mice when compared with WT, whereas oxytocin (OXT) basal mRNA levels were similar in both groups. Although the basal peripheral release of AVP and OXT was equivalent in both genotypes, we observed in KO mice a significant drop of AVP and OXT plasma values 15 min after stressor onset and a robust increase in the OXT plasma concentration at 60 min. These findings suggest that in the male mouse, NO inhibits AVP gene transcription in magnocellular neurones of the SON and collaborates in maintaining constant AVP and OXT plasma levels following acute stressor exposure, exerting a bimodal regulatory action on OXT secretion. We conclude that NO is involved in the regulation of magnocellular neurones of the SON, and it is preferentially implicated in the attenuation of the peripheral release of OXT induced by acute stressor exposure.
Nitric Oxide 2007 Feb
PMID:Neural nitric oxide gene inactivation affects the release profile of oxytocin into the blood in response to forced swimming. 1676 31

Oxytocin (OT; Cys-Tyr-Ile-Gln-Asn-Cys-Pro-leu-Gly), a posterior pituitary peptide hormone, is characterized by a Cys1-Cys6 disulfide bond in its stable, isolated state. This paper describes a simple, one-step method for the production of OT in its reduced, dithiol form (OT dithiol), free of reducing agent. The effects of temperature, pH, and metal-ion chelators on the autoxidation of OT dithiol were examined to establish if this form is likely to persist under biological conditions. It was found that OT dithiol has a half-life of 1.8h with respect to reformation of OT disulfide at 37 degrees C and pH 6.9 in the presence of the copper chelators, DTPA and neocuproine. S-Nitrosation of OT dithiol by acidified nitrite at pH 3.0 was examined by absorption spectroscopy and HPLC-UV-MS, which revealed that both singly and doubly S-nitrosated OT are formed. These results suggest novel chemical aspects to OT signaling, the biological implications of which are discussed here.
Nitric Oxide 2007 Sep
PMID:Reduction and S-nitrosation of the neuropeptide oxytocin: implications for its biological function. 1769 43

Bone marrow stem cells (BMSCs) express cardiac markers in vitro and in vivo upon induction. Cardiomyogenic differentiation of embryonic stem cells induced by oxytocin (OT) involves the nitric oxide (NO)-soluble guanylyl cyclase (sGC) pathway. Also, OT improved cardiomyogenic differentiation of porcine BMSCs (pBMSCs). Here, we document the role of NO pathway in OT-mediated cardiomyogenic differentiation of pBMSCs obtained from bone marrow aspirates of juvenile pigs. Cells were exposed (OT cells) or not (control cells) to OT, in presence or absence of a NO synthase inhibitor (L-NAME) and a sGC inhibitor (ODQ). Gene (RT-PCR) and protein expression (immunocytochemistry) of NOS was up-regulated after OT induction. Exposure of OT cells to L-NAME, ODQ, or both, leaded to a significant reduction in cardiac troponin I transcripts, and protein (Western Blot) expression. For the latter, ODQ looked more performing in inhibition than L-NAME. Expression of cardiac troponin T and myosin heavy chain (immunocytochemistry) was less abundant in OT cells exposed to inhibitors without apparent synergic effect between L-NAME and ODQ. In control cells, protein expression remained low. Moreover, OT-induced cell proliferation, and this effect was counteracted by NOS/sGC inhibitors. Inhibiting NO production and NO effector, sGC, affected the OT-mediated differentiation of pBMSCs, because abundance of cardiac proteins was reduced to levels similar to those observed in control cells. We propose that following treatment with OT, activation of NO pathway directs pBMSCs to a preferential cardiomyogenic phenotype and stimulates cell proliferation.
Nitric Oxide 2011 Jan 01
PMID:Involvement of the nitric oxide-soluble guanylyl cyclase pathway in the oxytocin-mediated differentiation of porcine bone marrow stem cells into cardiomyocytes. 2093 29

Full-term human umbilical cord contains three blood vessels: two arteries coiled around a vein and surrounded by Wharton's jelly, a mucous tissue with few mesenchymal stromal cells and abundant extracellular matrix. Umbilical vessels lack innervations, thus endothelial cells must play a role in the control of blood flow. The aim of this study was to investigate in human umbilical cord the expression of five peptides that could be involved in the regulation of vascular tone: Orphanin FQ, Oxytocin, Atrial Natriuretic Peptide (ANP), endothelial Nitric Oxide Synthase (eNOS) and inducible Nitric Oxide Synthase (iNOS). The expression of these molecules in full-term human umbilical cord was investigated through immunohistochemistry and RT-PCR. Immunoreactivity for Orphanin FQ was detected in Wharton's jelly, vessel musculature and endothelium; Oxytocin, ANP and eNOS were expressed by the umbilical epithelium, Wharton's jelly and endothelium, whereas iNOS only by endothelial cells. RT-PCR analysis showed transcriptional expression of Oxytocin, ANP and eNOS mRNAs. The presence of Orphanin, Oxytocin, ANP, eNOS and iNOS proteins was identified in the human umbilical cord. mRNA expression for Oxytocin, ANP and eNOS suggest that these molecules are synthesized by umbilical cord cells themselves. The expression of these vasoactive molecules could be part of a general mechanism locally regulating vascular tone.
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PMID:Human umbilical cord expresses several vasoactive peptides involved in the local regulation of vascular tone: protein and gene expression of Orphanin, Oxytocin, ANP, eNOS and iNOS. 2174 19