Disease relevance of Pip

• Antiestrogen inhibition of prolactin-induced growth of the Nb2 rat lymphoma cell line [1].
• The agonist LY379268 was able to prevent the transient hyperprolactinemia associated with stimulation of serotonin 5-HT2A receptors by 2,5-dimethoxy-4-iodoamphetamine (DOI), but did not alter the high levels of circulating prolactin induced with the D2 antagonist, haloperidol [2].
• Neuroanatomical specificity of prolactin-induced hyperphagia in virgin female rats [3].
• The decrease in pituitary prolactin induced by blinding and anosmia was reversed by pinealectomy or by the lower doses (1, 50 or 100 micrograms) of melatonin [4].
• Neonatal androgenization of the females significantly increased the release of prolactin induced by 5-HTP treatment compared to the values observed in males; thus, the neonatal exposure to androgens seems to be responsible for the sexual differences in the prolactin response to 5-HTP [5].

Psychiatry related information on Pip

• We explored the role of the opioid system and the participation of ovarian hormones in the regulation of prolactin induced by the suckling stimulus at the end of pregnancy in rats with developed maternal behavior, and during lactation [6].

High impact information on Pip

• Prolactin-induced cell proliferation in PC12 cells depends on JNK but not ERK activation [7].
• Further data indicate that two steroid hormones, hydrocortisone and progesterone, were able to modulate the prolactin-induced accumulation of casein mRNA [8].
• The transcription factor interferon regulatory factor-1 is expressed during both early G1 and the G1/S transition in the prolactin-induced lymphocyte cell cycle [9].
• Suppression of Prolactin-Induced Signal Transducer and Activator of Transcription 5b Signaling and Induction of Suppressors of Cytokine Signaling Messenger Ribonucleic Acid in the Hypothalamic Arcuate Nucleus of the Rat during Late Pregnancy and Lactation [10].
• Low concentrations of ethanol inhibits prolactin-induced mitogenesis and cytokine expression in cultured astrocytes [11].

Chemical compound and disease context of Pip

• Inhibition by genistein of prolactin-induced Nb2 lymphoma cell mitogenesis [12].

Biological context of Pip

• To address these questions, we dialyzed rats for 3 h in the supine position at constant levels of Pip with isotonic and hypertonic dialysis solutions containing a protein marker of fluid movement [13].
• Concomitant with the increase in MAP kinase activity, prolactin induced tyrosine phosphorylation in a number of liver proteins, suggesting a rapid involvement of tyrosine kinases which might be correlated in some way with MAP kinase activation [14].
• Endocytosis and degradation of ovine prolactin by Nb2 lymphoma cells: characterization and effects of agents known to alter prolactin-induced mitogenesis [15].
• We conclude that ICAM-1 expression and monocyte/macrophage accumulation are associated with prolactin-induced luteal regression in the rat and that these aspects are not influenced by testosterone [16].
• Progesterone on an oestrogen background enhances prolactin-induced apoptosis in regressing corpora lutea in the cyclic rat: possible involvement of luteal endothelial cell progesterone receptors [17].

Anatomical context of Pip

• Analogues of the superagonist [Sar1]ANGII with Aze or Pip at position 7 and sarcosine (Sar) or aminoisobutyric acid (Aib) at position 1 had high intrinsic activity in the rat isolated uterus assay (34-184%) [18].
• 5. It is concluded that on rat ganglia Pip is a nicotinic agonist, with no detectable GABA-mimetic activity [19].
• 1. The neuronal effects of the anthelmintic piperazine (Pip) on rat sympathetic ganglia were studied in vitro by means of intracellular and extracellular recording techniques [19].
• OBJECTIVES: To investigate the effect of simultaneous exposure of anterior abdominal muscle (AAM) to changes in intraperitoneal hydrostatic pressure (Pip) and to osmolality of peritoneal fluid on total tissue water (TTW) and on the pattern of distribution of TTW in the AAM [20].
• Measurements of the interstitial pressure gradient in the abdominal wall demonstrated minimal change when Pip was increased from 0 to 8 mmHg [21].

Associations of Pip with chemical compounds

• Analogues of Sarmesin ([Sar1,Tyr-(OMe)4]ANGII) with Aze and Pip at position 7 had pA2 values of 7.4 and 6.5, respectively [18].
• Synthesis and biological activities of angiotensin II, Sarilesin, and Sarmesin analogues containing Aze or Pip at position 7 [18].
• Analogues of [Sar1]angiotensin II, Sarilesin (type I antagonist), and Sarmesin (type II antagonist) with L-azetidine-2-carboxylic acid (Aze) and L-pipecolic acid (Pip) at position 7 have been prepared by the solid-phase method, purified by reverse-phase HPLC, and bioassayed in the rat uterus [18].
• Depolarizations produced by Pip or carbachol (but not GABA) were markedly depressed by hexamethonium but only slightly by bicuculline or picrotoxin [19].
• 4. In the presence of hexamethonium (1 mM), the responses to Pip hexahydrate and to cholinoceptor agonists were abolished, but Pip citrate still changed the spike configuration and induced membrane hyperpolarization with a small conductance increase [19].

Regulatory relationships of Pip

• The results reconfirm the possible role of noradrenergic neurons in the release of prolactin induced by EB and also suggest that EB stimulates a dopaminergic mechanism which is inhibitory to prolactin release but is normally masked by increased noradrenergic activity [22].

Other interactions of Pip

• Signal transducer and activator of transcription-5 (Stat5) is known to play a critical role in prolactin-induced beta-casein gene transcription in rodents [23].
• Serotonin also enhanced the release of prolactin induced by 30 nmol/l thyrotropin-releasing hormone (TRH), at all doses tested [24].
• Synergistic gene expressions of cyclin E, cdk2, cdk5 and E2F-1 during the prolactin-induced G1/S transition in rat Nb2 pre-T lymphoma cells [25].
• Since the presence of prolactin receptors was earlier demonstrated in hypothalamic dopaminergic neurons, our working hypothesis was that prolactin induced activation of prolactin receptor coupled signaling leads to increased neuronal activity in these neurons [26].
• The aim of this study was to correlate prolactin receptor mediated signaling and prolactin induced activation in hypothalamic dopaminergic neurons [26].

Analytical, diagnostic and therapeutic context of Pip

• RESULTS: Regardless of the osmolality of the dialysis solution, elevation of Pip to 6 mmHg results in tissue expansion, primarily in theta(if), which is doubled to 1.71+/-0.11 mL/g dry weight and 1.60+/-0.17 mL/g dry weight with isotonic and hypertonic dialysis, respectively, as compared to controls (0.64+/-0.04 mL/g dry weight) [20].
• To test this hypothesis, we used dual-label quantitative autoradiography (QAR) to measure extracellular fluid volume (thetaec) and intravascular volume (thetaiv) in the AAM of rats within the Pip range from -2.8 to +8 mmHg. thetaif was obtained by subtraction (thetaec - thetaiv). dPif/dx was measured with a micropipette and a servo-null system [27].
• The results demonstrate that ovine prolactin-induced suppression of LH secretion after castration occurs with or without the adrenal glands [28].
• Differential effects of adrenalectomy on the prolactin-induced suppression of LH and FSH secretion after castration in male rats [28].
• Prolactin-induced structural luteolysis was associated with apoptosis verified by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) [29].

References