Neuropeptide variability in man

Onuoha, Gracey N.; Nugent, A. M.; Hunter, Steven; Alpar, E. K.; McEneaney, D.; Campbell, N. P. S.; Shaw, Christopher; Buchanan, K.D.; Nicholls, D. P.

doi:10.1046/j.1365-2362.2000.00676.x

Cited by 18 publications

(14 citation statements)

References 38 publications

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“…The displacement studies indicate that Y5R has two binding sites to NPY and Y5R-SAP, suggesting that this receptor binds its ligands with high and low affinity. In humans, the circulating levels of NPY (33), , and PP peptides (35) Analysis of signaling pathways in BT-549 cells revealed that Y5R activation is coupled to cAMP inhibition but not to intracellular Ca 2+ signaling pathway. Previous studies have shown that activation of Y5R in transfected HEC-1B cells had no effect on intracellular Ca 2+ mobilization but inhibited forskolin-induced cAMP accumulation (36).…”

Section: Discussionmentioning

confidence: 99%

Neuropeptide Y Y5 Receptor Promotes Cell Growth through Extracellular Signal-Regulated Kinase Signaling and Cyclic AMP Inhibition in a Human Breast Cancer Cell Line

Sheriff

Ali

Yahya

et al. 2010

Molecular Cancer Research

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Overexpression of neuropeptide Y (NPY) and its receptor system has been reported in various types of cancers. NPY Y5 receptor (Y5R) has been implicated in cell growth and angiogenesis. However, the role of Y5R in breast cancer is unknown. To identify the role of Y5R in breast cancer, we screened several breast cancer cell lines to examine the expression of Y5R and its function in breast cancer. All screened cell lines express both Y1 receptor and Y5R except BT-549, which expresses mainly Y5R. Binding studies showed that NPY, Y5R-selective agonist peptide, and Y5R-selective antagonist (CGP71683A) displaced

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Section: Discussionmentioning

confidence: 99%

Neuropeptide Y Y5 Receptor Promotes Cell Growth through Extracellular Signal-Regulated Kinase Signaling and Cyclic AMP Inhibition in a Human Breast Cancer Cell Line

Sheriff

Ali

Yahya

et al. 2010

Molecular Cancer Research

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“…The increased Ang-(1-12) expression was associated with high left atrium chymase activity [76]. A differential content or expression of endocrine peptides in the heart has been reported in several species [77;78]. In all species studied including humans, right atrial tissue concentrations of atrial natriuretic peptide are at least two-fold higher in the right compared to the left atrium [77].…”

Section: Novel Pathways Upstream From Angiotensin I –The New Research–mentioning

confidence: 99%

An evolving story of angiotensin-II-forming pathways in rodents and humans

et al. 2013

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Lessons learned from the characterization of the biological roles of angiotensin-(1-7) in opposing the vasoconstrictor, proliferative, and prothrombotic actions of angiotensin II created an underpinning for a more comprehensive exploration of the multiple pathways by which the blood and tissues renin angiotensin system regulates homeostasis and its altered state in disease processes. This review summarizes the progress that has been made in the novel exploration of intermediate shorter forms of angiotensinogen through the characterization of the expression and functions of the dodecapeptide angiotensin-(1-12) in the cardiac production of angiotensin II. The studies reveal significant differences in humans versus rodents regarding the enzymatic pathway by which angiotensin-(1-12) undergoes metabolism. Highlights of the research include the demonstration of chymase-direct formation of angiotensin II from angiotensin-(1-12) in human left atrial myocytes and left ventricular tissue, the presence of robust expression of angiotensin-(1-12) and chymase in the atrial appendage of subjects with resistant atrial fibrillation, and the preliminary observation of significantly higher angiotensin-(1-12) expression in human left atrial appendages.

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“…Also, NPY may have a role in processes leading to decompensation and deterioration to overt heart failure. Several pertinent reports have demonstrated elevated plasma levels of NPY, regardless of the etiology [31][32][33][34], and these have prognostic significance for severity of disease and outcome [35]. As a potent vasoconstricting agent, NPY can produce coronary artery constriction and spasm, possibly contributing to myocardial ischemia and infarction.…”

Section: Introductionmentioning

confidence: 99%

NPY and Cardiac Diseases

McDermott¹,

Bell²

2007

CTMC

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Hypertension-induced left ventricular hypertrophy (LVH), along with ischemic heart disease, result in LV remodeling as part of a continuum that often leads to congestive heart failure. The neurohormonal model has been used to underpin many treatment strategies, but optimal outcomes have not been achieved. Neuropeptide Y (NPY) has emerged as an additional therapeutic target, ever since it was recognised as an important mediator released from sympathetic nerves in the heart, affecting coronary artery constriction and myocardial contraction. More recent interest has focused on the mitogenic and hypertrophic effects that are observed in endothelial and vascular smooth muscle cells, and cardiac myocytes. Of the six identified NPY receptor subtypes, Y(1), Y(2) and Y(5) appear to mediate the main functional responses in the heart. Plasma levels of NPY become elevated due to the increased sympathetic activation present in stress-related cardiac conditions. Also, NPY and Y receptor polymorphisms have been identified that may predispose individuals to increased risk of hypertension and cardiac complications. This review examines what understanding exists regarding the likely contribution of NPY to cardiac pathology. It appears that NPY may play a part in compensatory or detrimental remodeling of myocardial tissue subsequent to hemodynamic overload or myocardial infarction, and in angiogenic processes to regenerate myocardium after ischemic injury. However, greater mechanistic information is required in order to truly assess the potential for treatment of cardiac diseases using NPY-based drugs.

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Neuropeptide variability in man

Cited by 18 publications

References 38 publications

Neuropeptide Y Y5 Receptor Promotes Cell Growth through Extracellular Signal-Regulated Kinase Signaling and Cyclic AMP Inhibition in a Human Breast Cancer Cell Line

Neuropeptide Y Y5 Receptor Promotes Cell Growth through Extracellular Signal-Regulated Kinase Signaling and Cyclic AMP Inhibition in a Human Breast Cancer Cell Line

An evolving story of angiotensin-II-forming pathways in rodents and humans

NPY and Cardiac Diseases

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