Expression of neuropeptide Y and its receptors Y1 and Y2 in the rat heart and its supplying autonomic and spinal sensory ganglia in experimentally induced diabetes

Dvoráková, Magdalena Chottová; Wiegand, Silke; Pešta, Martin; Slavikova, Jana; Grau, Veronika; Reischig, Josef; Kuncová, Jitka; Kummer, Wolfgang

doi:10.1016/j.neuroscience.2007.07.069

Cited by 32 publications

(23 citation statements)

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“…Furthermore, the Y1 receptors appeared to be preferentially expressed in the nuclei of cardiomyocytes and vascular smooth muscle cells. The same phenomenon was also shown to exist in animal models of chronic hyperglycemia [124] and may occur because of the counter regulation response to reduced levels of NPY. However, whether these alterations in NPY and its receptors are associated with the initial etiology of disease in the myocardium requires further investigation.…”

Section: The Characteristics Of Human Npy Receptorsmentioning

confidence: 76%

“…In the myocardium of the diabetic rat, the expression of NPY was shown to be different than other tissues and its receptors were up-regulated [124]. In the cardiovascular system, NPY is co-expressed and co-exists predominantly in the coronary arteries, endothelium [122] and cardiomyocytes innervated by sympathetic nerves together with other classic neurotransmitters such as sympathetic noradrenaline.…”

Section: The Characteristics Of Human Npy Receptorsmentioning

confidence: 99%

“…In the cardiovascular system, NPY is co-expressed and co-exists predominantly in the coronary arteries, endothelium [122] and cardiomyocytes innervated by sympathetic nerves together with other classic neurotransmitters such as sympathetic noradrenaline. NPY receptors, particularly the Y1 and Y2 receptors, have been demonstrated to play a fundamental role in the pathogenesis of myocardial hypertrophy in the rat [124]. Indeed, NPY Y1 receptor expression was elevated in rat myocardium leading to hypertrophy of the cardiac myocytes via reduced degradation and the increased synthesis of protein via PI3K/p70 signaling pathways [125].…”

Section: The Characteristics Of Human Npy Receptorsmentioning

confidence: 99%

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A Promising Therapeutic Target for Metabolic Diseases: Neuropeptide Y Receptors in Humans

et al. 2017

Cell Physiol Biochem

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Human neuropeptide Y (hNPY) is one of the most widely expressed neurotransmitters in the human central and peripheral nervous systems. It consists of 36 highly conserved amino acid residues, and was first isolated from the porcine hypothalamus in 1982. While it is the most recently discovered member of the pancreatic polypeptide family (which includes neuropeptide Y, gut-derived hormone peptide YY, and pancreatic polypeptide), NPY is the most abundant peptide found in the mammalian brain. In order to exert particular functions, NPY needs to bind to the NPY receptor to activate specific signaling pathways. NPY receptors belong to the class A or rhodopsin-like G-protein coupled receptor (GPCR) family and signal via cell-surface receptors. By binding to GPCRs, NPY plays a crucial role in various biological processes, including cortical excitability, stress response, food intake, circadian rhythms, and cardiovascular function. Abnormal regulation of NPY is involved in the development of a wide range of diseases, including obesity, hypertension, atherosclerosis, epilepsy, metabolic disorders, and many cancers. Thus far, five receptors have been cloned from mammals (Y1, Y2, Y4, Y5, and y6), but only four of these (hY1, hY2, hY4, and hY5) are functional in humans. In this review, we summarize the structural characteristics of human NPY receptors and their role in metabolic diseases.

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Section: The Characteristics Of Human Npy Receptorsmentioning

confidence: 76%

Section: The Characteristics Of Human Npy Receptorsmentioning

confidence: 99%

Section: The Characteristics Of Human Npy Receptorsmentioning

confidence: 99%

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A Promising Therapeutic Target for Metabolic Diseases: Neuropeptide Y Receptors in Humans

et al. 2017

Cell Physiol Biochem

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“…Amplification of cDNA by PCR was performed using the HotStartTaq Master Mix Kit (Qiagen). The primers used were: NPY (NM_012614), 5Ј-GGCCAGATACTACTCCGCTCTGCG-3Ј (forward) and 5Ј-TTCACAGGATGAGATGAGATGTG-3Ј (reverse) (Chottova Dvorakova et al, 2008); PYY (NM_001034080), 5Ј-CTCTGTTCTCCAAACTGCTC-3Ј (forward) and 5Ј-ACCAAACATGCAAGTGAAGTC-3Ј (reverse); PP (NM_012626), 5Ј-CATACTACTGCCTCTCCCTG-3Ј (forward) and 5Ј-GTTTCGTATTGAGCCCTCTG-3Ј (reverse); NPY Y1 receptor (X95507), 5Ј-AAATGTATCACTTGCGGCGTTCA-3Ј (forward) and 5Ј-GCGACCACGATGGAGAGCAG-3Ј (reverse) (Jackerott and Larsson, 1997), Y2 receptor (NM_023968), 5Ј-CCCGGATCTGGAGTAAGCTAAA-3Ј (forward) and 5Ј-GTGGAGCACATCGCAATAATGT-3Ј (reverse) (Chottova Dvorakova et al, 2008); Y4 receptor (NM_031581), 5Ј-TTGCAGTTCTCTGGCTGCCCCTG-3Ј (forward) and 5Ј-CTTGCTACCCATCCTCATAGAT-3Ј (reverse); Y5 receptor (NM_012869), 5Ј-CCAGGCAAAAACCCCCAGCAC-3Ј (forward) and 5Ј-GGCAGTGGATAAGGGCTCTCA-3Ј (reverse); and -actin (NM_031144), 5Ј-TCATCACTATCGGCAATGAGC-3Ј (forward) and 5Ј-CTCCTTCTGCATCCTGTCAGC-3Ј (reverse).…”

Section: Rt-pcrmentioning

confidence: 99%

Neuropeptide Y functions as a facilitator of GDNF-induced budding of the Wolffian duct

et al. 2009

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Ureteric bud (UB) emergence from the Wolffian duct (WD), the initiating step in metanephric kidney morphogenesis, is dependent on GDNF; however, GDNF by itself is generally insufficient to induce robust budding of the isolated WD in culture. Thus, additional factors, presumably peptides or polypeptide growth factors, might be involved. Microarray data from in vivo budding and nonbudding conditions were analyzed using non-negative matrix factorization followed by gene ontology filtering and network analysis to identify sets of genes that are highly regulated during budding. These included the GDNF co-receptors GFR1 and RET, as well as neuropeptide Y (NPY). By using ANOVA with pattern matching, NPY was also found to correlate most significantly to the budded condition with a high degree of connectedness to genes with developmental roles. Exogenous NPY [as well as its homolog, peptide YY (PYY)] augmented GDNF-dependent budding in the isolated WD culture; conversely, inhibition of NPY signaling or perturbation of NPY expression inhibited budding, confirming that NPY facilitates this process. NPY was also found to reverse the decreased budding, the downregulation of RET expression, the mislocalization of GFR1, and the inhibition of AKT phosphorylation that resulted from the addition of BMP4 to the isolated WD cultures, suggesting that NPY acts through the budding pathway and is reciprocally regulated by GDNF and BMP4. Thus, the outgrowth of the UB from the WD might result from a combination of the upregulation of the GDNF receptors together with genes that support GDNF signaling in a feed-forward loop and/or counteraction of the inhibitory pathway regulated by BMP4.

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“…eNOS uncoupling leading to nitrosative stress and formation of peroxynitrite induces damage of neuronal axons, which are particularly prone to oxidative and nitrosative stress due to their high mitochondrial content [82]. This leads to a prominent abnormality in the levels of cardioactive neuropeptides including neuropeptide Y, substance P [83], calcitonin-generated peptide, natriuretic peptides (ANP, BNP, and C-type natriuretic peptide) [84] as well as the respective neuropeptide effectors [85], contributing to impaired endothelium-dependent vasodilation in HFpEF [86]. This limits the delivery and extraction of tissue oxygen, which subsequently results in nerve hypoxia and impaired nerve function [80].…”

Section: Introductionmentioning

confidence: 99%

New Insights in (Inter)Cellular Mechanisms by Heart Failure with Preserved Ejection Fraction

Tschöpe

Linthout

2014

Curr Heart Fail Rep

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Recently, a new paradigm for the development of heart failure with preserved ejection fraction (HFpEF) has been proposed, which identifies a systemic pro-inflammatory state induced by comorbidities as the origin of microvascular endothelial cell inflammation and subsequent concentric cardiac remodeling and dysfunction. This review further discusses the pivotal role of the inflamed endothelium in the pathogenesis of HFpEF-specific cardiac remodeling. The potential importance of reciprocal interactions of the endothelium with cardiac fibroblasts and cardiomyocytes and with the cardiac neurohumoral response in this cardiac remodeling process is outlined.

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Expression of neuropeptide Y and its receptors Y1 and Y2 in the rat heart and its supplying autonomic and spinal sensory ganglia in experimentally induced diabetes

Cited by 32 publications

References 53 publications

A Promising Therapeutic Target for Metabolic Diseases: Neuropeptide Y Receptors in Humans

A Promising Therapeutic Target for Metabolic Diseases: Neuropeptide Y Receptors in Humans

Neuropeptide Y functions as a facilitator of GDNF-induced budding of the Wolffian duct

New Insights in (Inter)Cellular Mechanisms by Heart Failure with Preserved Ejection Fraction

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