scholarly journals Placental Neuropeptide Y (NPY) and NPY receptors expressions and serum NPY levels in preeclampsia

2019 ◽  
Vol 244 (5) ◽  
pp. 380-388 ◽  
Author(s):  
Roongrit Klinjampa ◽  
Chantacha Sitticharoon ◽  
Xaynaly Souvannavong-Vilivong ◽  
Chanakarn Sripong ◽  
Issarawan Keadkraichaiwat ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Gestational Age ◽  
Receptor Expression ◽  
Clinical Parameters ◽  
Expression Ratio ◽  
Y1 Receptor ◽  
Placental Angiogenesis ◽  
Y2 Receptor ◽  
Npy Receptor ◽  
Npy Receptors

Neuropeptide Y (NPY) has been reported as a vasoconstrictive substance that might be associated with preeclampsia. NPY mediates different effects via its specific NPY receptors. NPY action via Y1 receptor (Y1R) and/or Y5 receptor (Y5R) induces vascular smooth muscle cells proliferation while it is implicated in angiogenesis via Y2 receptor (Y2R) and/or Y5R. The objectives of this study were to (1) compare placental NPY, Y1 receptor ( Y1R), Y2 receptor ( Y2R), and Y5 receptor ( Y5R) expressions between normal (NP) and preeclamptic (PE) pregnancies to determine whether gene expression of different NPY receptors are altered in the PE condition; (2) compare maternal serum NPY levels between NP and PE subjects; and (3) determine correlations between placental gene expressions as well as serum NPY levels with maternal and neonatal clinical parameters. There were 22 subjects each in the NP (gestational age 37–42 weeks) and PE (gestational age ≥34 weeks) groups. Clinical parameters and serum NPY levels were measured before delivery. NPY expression and serum NPY levels were comparable between NP and PE subjects. Y1R, Y2R, and Y5R expressions were significantly lower in PE than NP subjects. In all and NP subjects, placental Y2R showed the highest expression, tended to be higher than Y5R, and was significantly higher than Y1R. In PE subjects, placental Y2R was comparable to Y5R and both Y2R and Y5R were significantly higher than Y1R. The NPY receptor expression ratio between the PE/NP groups showed that it was lowest for Y2R (0.27) compared to Y1R (0.42) and Y5R (0.40) suggestive of decreased Y2R expression in PE subjects. In summary, a decrease in placental Y2R mRNA might be associated with abnormalities of placental angiogenesis which probably contributes to the pathophysiology of preeclampsia. The roles of NPY receptors mediating placental vascularization need to be further investigated. Impact statement Neuropeptide Y (NPY) has been reported as a vasoconstrictive substance which might be associated with preeclampsia. The novel findings of this study were that Y1R, Y2R, and Y5R expressions were significantly lower in the PE than the NP group. Moreover, the NPY receptor expression ratio between the PE/NP groups was lowest for Y2R (0.27) compared to Y1R (0.42) and Y5R (0.40) suggestive of a reduction of this receptor in the preeclampsia group. Our results suggested that decreased Y2R mRNA in the PE group might be associated with abnormalities of placental angiogenesis which probably contributes to the pathophysiology of preeclampsia.

Distribution and activity of dogfish NPY and peptide YY in the cardiovascular system of the common dogfish

1993 ◽  
Vol 264 (6) ◽  
pp. R1119-R1124 ◽  
Author(s):  
C. Bjenning ◽  
N. Hazon ◽  
A. Balasubramaniam ◽  
S. Holmgren ◽  
J. M. Conlon
Keyword(s):  
Neuropeptide Y ◽  
Cardiovascular System ◽  
Peptide Yy ◽  
Nerve Fibers ◽  
Dependent Manner ◽  
Cardiovascular Tissue ◽  
Y1 Receptor ◽  
Selective Agonist ◽  
Y2 Receptor ◽  
The Common

Neuropeptide Y is present in sympathetic nerves in the mammalian cardiovascular system. This study has investigated the distribution of neuropeptide Y in the cardiovascular and gastrointestinal systems and the effect of dogfish neuropeptide Y and related peptides on cardiovascular tissue of an elasmobranch fish, the common dogfish (Scyliorhinus canicula). Neuropeptide Y-like immunoreactivity is present in varicose nerve fibers innervating dogfish gut and cardiovascular tissue and in endocrine cells of the dogfish spiral intestine. Dogfish neuropeptide Y, dogfish peptide YY, and porcine neuropeptide Y contract the dogfish afferent branchial artery in a concentration-dependent manner. The effect is not inhibited by the presence of tetrodotoxin or by removal of the endothelium. The mammalian Y1 receptor selective agonist [Leu31Pro34]NPY but not the mammalian Y2 receptor selective agonist neuropeptide Y-(13-36) peptide has vasoconstrictor properties in this system, suggesting that the receptor mediating the vasoconstriction resembles the mammalian Y1 receptor more than the Y2 receptor.

scholarly journals Basomedial Hypothalamic Injections of Neuropeptide Y Conjugated to Saporin Selectively Disrupt Hypothalamic Controls of Food Intake

Endocrinology ◽  
2005 ◽  
Vol 146 (3) ◽  
pp. 1179-1191 ◽  
Author(s):  
Kishor Bugarith ◽  
Thu T. Dinh ◽  
Ai-Jun Li ◽  
Robert C. Speth ◽  
Sue Ritter
Keyword(s):  
Neuropeptide Y ◽  
Arcuate Nucleus ◽  
Retrograde Transport ◽  
Related Protein ◽  
Y1 Receptor ◽  
Npy Receptor ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Glucoprivic Feeding ◽  
Agouti Gene

Neuropeptide Y (NPY) conjugated to saporin (NPY-SAP), a ribosomal inactivating toxin, is a newly developed compound designed to selectively target and lesion NPY receptor-expressing cells. We injected NPY-SAP into the basomedial hypothalamus (BMH), just dorsal to the arcuate nucleus (ARC), to investigate its neurotoxicity and to determine whether ARC NPY neurons are required for glucoprivic feeding. We found that NPY-SAP profoundly reduced NPY Y1 receptor and αMSH immunoreactivity, as well as NPY, Agouti gene-related protein (AGRP), and cocaine and amphetamine-related transcript mRNA expression in the BMH. NPY-SAP lesions were localized to the injection site with no evidence of retrograde transport by hindbrain NPY neurons with BMH terminals. These lesions impaired responses to intracerebroventricular (icv) leptin (5 μg/5 μl·d) and ghrelin (2 μg/5 μl), which are thought to alter feeding primarily by actions on ARC NPY/AGRP and proopiomelanocortin/cocaine and amphetamine-related transcript neurons. However, the hypothesis that NPY/AGRP neurons are required downstream mediators of glucoprivic feeding was not supported. Although NPY/AGRP neurons were destroyed by NPY-SAP, the lesion did not impair either the feeding or the hyperglycemic response to 2-deoxy-d-glucose-induced blockade of glycolysis use. Similarly, responses to glucagon-like peptide-1 (GLP-1, 5 μg/3 μl icv), NPY (5 μg/3 μl icv), cholecystokinin octapeptide (4 μg/kg ip), and β-mercaptoacetate (68 mg/kg ip) were not altered by the NPY-SAP lesion. Thus, NPY-SAP destroyed NPY receptor-expressing neurons in the ARC and selectively disrupted controls of feeding dependent on those neurons but did not disrupt peptidergic or metabolic controls dependent upon circuitry outside the BMH.

Food intake regulation in rodents: Y5 or Y1 NPY receptors or both?

2000 ◽  
Vol 78 (2) ◽  
pp. 173-185 ◽  
Author(s):  
Jacques Duhault ◽  
Michèle Boulanger ◽  
Susana Chamorro ◽  
Jean A Boutin ◽  
Odile Della Zuana ◽  
...  
Keyword(s):  
Food Intake ◽  
Neuropeptide Y ◽  
Inhibitory Effect ◽  
Receptor Subtype ◽  
Pharmacological Characterization ◽  
Npy Receptor ◽  
Obesity Drugs ◽  
Npy Receptors

Neuropeptide Y (NPY), one of the most abundant peptides in rat and human brains, appears to act in the hypothalamus to stimulate feeding. It was first suggested that the NPY Y1 receptor (Y1R) was involved in feeding stimulated by NPY. More recently a novel NPY receptor subtype (Y5R) was identified in rat and human as the NPY feeding receptor subtype. There is, however, no absolute consensus since selective Y1R antagonists also antagonize NPY-induced hyperphagia. Nevertheless, new anti-obesity drugs may emerge from further pharmacological characterization of the NPY receptors and their antagonists. A large panel of Y1R and Y5R antagonists (such as CGP71683A, BIBO3304, BIBP3226, 1229U91, and SYNAPTIC and BANYU derivatives but also patentable in-house-synthesized compounds) have been evaluated through in vitro and in vivo tests in an attempt to establish a predictive relationship between the binding selectivity for human receptors, the potency in isolated organs assays, and the inhibitory effect on food intake in both normal and obese hyperphagic rodents. Although these results do not allow one to conclude on the implication of a single receptor subtype at the molecular level, this approach is crucial for the design of novel NPY receptor antagonists with potential use as anti-obesity drugs and for evaluation of their possible adverse peripheral side effects, such as hypotension.Key words: obesity, weight reduction, food intake, neuropeptide Y, rodents.

Peptide YY/neuropeptide Y Y1 receptor expression in the epithelium and mucosal nerves of the human colon

1999 ◽  
Vol 83 (1) ◽  
pp. 11-19 ◽  
Author(s):  
Peter J Mannon ◽  
Anuradha Kanungo ◽  
Roslyn B Mannon ◽  
Kirk A Ludwig
Keyword(s):  
Neuropeptide Y ◽  
Peptide Yy ◽  
Human Colon ◽  
Receptor Expression ◽  
Y1 Receptor

scholarly journals Central nervous system neuropeptide Y signaling via the Y1 receptor partially dissociates feeding behavior from lipoprotein metabolism in lean rats

2012 ◽  
Vol 303 (12) ◽  
pp. E1479-E1488 ◽  
Author(s):  
Jennifer M. Rojas ◽  
John M. Stafford ◽  
Sanaz Saadat ◽  
Richard L. Printz ◽  
Annette G. Beck-Sickinger ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Food Intake ◽  
Neuropeptide Y ◽  
Feeding Behavior ◽  
Receptor Agonist ◽  
Receptor Agonists ◽  
Y1 Receptor ◽  
Y2 Receptor ◽  
Long Evans

Elevated plasma triglyceride (TG) levels contribute to an atherogenic dyslipidemia that is associated with obesity, diabetes, and metabolic syndrome. Numerous models of obesity are characterized by increased central nervous system (CNS) neuropeptide Y (NPY) tone that contributes to excess food intake and obesity. Previously, we demonstrated that intracerebroventricular (icv) administration of NPY in lean fasted rats also elevates hepatic production of very low-density lipoprotein (VLDL)-TG. Thus, we hypothesize that elevated CNS NPY action contributes to not only the pathogenesis of obesity but also dyslipidemia. Here, we sought to determine whether the effects of NPY on feeding and/or obesity are dissociable from effects on hepatic VLDL-TG secretion. Pair-fed, icv NPY-treated, chow-fed Long-Evans rats develop hypertriglyceridemia in the absence of increased food intake and body fat accumulation compared with vehicle-treated controls. We then modulated CNS NPY signaling by icv injection of selective NPY receptor agonists and found that Y1, Y2, Y4, and Y5 receptor agonists all induced hyperphagia in lean, ad libitum chow-fed Long-Evans rats, with the Y2 receptor agonist having the most pronounced effect. Next, we found that at equipotent doses for food intake NPY Y1 receptor agonist had the most robust effect on VLDL-TG secretion, a Y2 receptor agonist had a modest effect, and no effect was observed for Y4 and Y5 receptor agonists. These findings, using selective agonists, suggest the possibility that the effect of CNS NPY signaling on hepatic VLDL-TG secretion may be relatively dissociable from effects on feeding behavior via the Y1 receptor.

Y1 and Y2 Receptor Selective Neuropeptide Y Analogs: Evidence for a Y1 Receptor Subclass

1995 ◽  
Vol 38 (22) ◽  
pp. 4579-4586 ◽  
Author(s):  
Dean A. Kirby ◽  
Steven C. Koerber ◽  
John M. May ◽  
Cristin Hagaman ◽  
Mary Jane Cullen ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Y1 Receptor ◽  
Y2 Receptor

scholarly journals Autoreceptor-induced inhibition of neuropeptide Y release from PC-12 cells is mediated by Y2 receptors

1997 ◽  
Vol 273 (4) ◽  
pp. H1737-H1744 ◽  
Author(s):  
Xiaoli Chen ◽  
Debora A. Dimaggio ◽  
Song Ping Han ◽  
Thomas C. Westfall
Keyword(s):  
Neuropeptide Y ◽  
Peptide Yy ◽  
Dependent Manner ◽  
Inhibitory Effects ◽  
Ideal Model ◽  
Concentration Dependent Manner ◽  
Pc 12 Cells ◽  
Npy Receptor ◽  
Neuropeptide Y Release ◽  
Npy Receptors

Pheochromocytoma (PC)-12 cells express Y1, Y2, and Y3 neuropeptide Y (NPY) receptors when differentiated with nerve growth factor (NGF). The present work evaluated NGF-differentiated PC-12 cells as a model system to study modulation of NPY release by NPY autoreceptors. We demonstrated that both K+ and nicotine stimulated concomitant release of NPY and dopamine from differentiated PC-12 cells. We also showed in this study that NPY release from PC-12 cells was attenuated in a concentration-dependent manner by peptide YY (PYY)-(13—36), a selective agonist for the Y2 type of NPY receptors. This result demonstrated that NPY release could be modulated by NPY autoreceptors of the Y2 subtype. The inhibitory action of PYY-(13—36) may be mediated at least in part by inhibition of N-type Ca2+channels, because PYY-(13—36) could not produce further inhibitory effects in the presence of a maximum effective concentration of ω-conotoxin, an N-type Ca2+-channel blocker. The inhibition by PYY-(13—36) could be blocked by pretreatment of cells with pertussis toxin, suggesting that an inhibitory GTP-binding protein was involved. Furthermore, the function of NPY autoreceptors could be modulated by other receptors such as β-adrenergic and ATP receptors. The evoked release of NPY was also attenuated by ATP and adenosine, which have been shown to be colocalized and coreleased with NPY from sympathetic nerve terminals. These results suggest that PC-12 cells differentiated with NGF may be an ideal model to study regulatory mechanisms of NPY release and that autoreceptor-mediated regulation of NPY release appears to act through the Y2 subtype of the NPY receptor.

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