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https://www.readbyqxmd.com/read/29670288/structural-basis-of-ligand-binding-modes-at-the-neuropeptide-y-y-1-receptor
#1
Zhenlin Yang, Shuo Han, Max Keller, Anette Kaiser, Brian J Bender, Mathias Bosse, Kerstin Burkert, Lisa M Kögler, David Wifling, Guenther Bernhardt, Nicole Plank, Timo Littmann, Peter Schmidt, Cuiying Yi, Beibei Li, Sheng Ye, Rongguang Zhang, Bo Xu, Dan Larhammar, Raymond C Stevens, Daniel Huster, Jens Meiler, Qiang Zhao, Annette G Beck-Sickinger, Armin Buschauer, Beili Wu
Neuropeptide Y (NPY) receptors belong to the G-protein-coupled receptor superfamily and have important roles in food intake, anxiety and cancer biology 1,2 . The NPY-Y receptor system has emerged as one of the most complex networks with three peptide ligands (NPY, peptide YY and pancreatic polypeptide) binding to four receptors in most mammals, namely the Y1 , Y2 , Y4 and Y5 receptors, with different affinity and selectivity 3 . NPY is the most powerful stimulant of food intake and this effect is primarily mediated by the Y1 receptor (Y1 R) 4 ...
April 18, 2018: Nature
https://www.readbyqxmd.com/read/29523877/diet-induced-obesity-suppresses-cortical-bone-accrual-by-a-neuropeptide-y-dependent-mechanism
#2
Natalie K Y Wee, Ronaldo F Enriquez, Amy D Nguyen, Harry Horsnell, Rishikesh Kulkarni, Ee Cheng Khor, Herbert Herzog, Paul A Baldock
OBJECTIVE: To determine whether age and neuropeptide Y (NPY) were involved in the skeletal response to extended periods of diet-induced obesity. METHODS: Male wild-type (WT) and NPY null (NPYKO) mice were fed a mild (23% fat) high-fat diet for 10 weeks from 6 or 16 weeks of age. Metabolism and bone density were assessed during feeding. Skeletal changes were assessed by microCT and histomorphometry. RESULTS: High-fat feeding in 6-week-old WT mice led to significantly increased body weight, adiposity and serum leptin levels, accompanied with markedly suppressed cortical bone accrual...
March 9, 2018: International Journal of Obesity: Journal of the International Association for the Study of Obesity
https://www.readbyqxmd.com/read/29477253/central-rank-signalling-in-npy-neurons-alters-bone-mass-in-male-mice
#3
N J Lee, I M Clarke, R F Enriquez, V Nagy, J Penninger, P A Baldock, H Herzog
RANKL signalling known to be important for the control of bone mass, has recently also been implicated in the brain to control thermoregulation, however, it is not known which neuronal pathways are involved and whether other aspects of energy homeostasis are also affected. Here we show that selective deletion of RANK from NPY neurons down-regulated NPY mRNA expression in the hypothalamus. While comprehensive phenotyping of germline-induced NPY neuron specific RANK deficient mice revealed no significant changes in physical or metabolic parameters, adult onset deletion of RANK from NPY neurons led to a significant increase in fat mass and a decrease in whole body bone mineral content and bone mineral density...
February 15, 2018: Neuropeptides
https://www.readbyqxmd.com/read/29373492/do-neuroendocrine-peptides-and-their-receptors-qualify-as-novel-therapeutic-targets-in-osteoarthritis
#4
REVIEW
Susanne Grässel, Dominique Muschter
Joint tissues like synovium, articular cartilage, meniscus and subchondral bone, are targets for neuropeptides. Resident cells of these tissues express receptors for various neuroendocrine-derived peptides including proopiomelanocortin (POMC)-derived peptides, i.e., α-melanocyte-stimulating hormone (α-MSH), adrenocorticotropin (ACTH) and β-endorphin (β-ED), and sympathetic neuropeptides like vasoactive intestinal peptide (VIP) and neuropeptide y (NPY). Melanocortins attained particular attention due to their immunomodulatory and anti-inflammatory effects in several tissues and organs...
January 26, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29130939/open-the-gates-vascular-neurocrine-signaling-mobilizes-hematopoietic-stem-and-progenitor-cells
#5
Tomer Itkin, Jesús María Gómez-Salinero, Shahin Rafii
Mobilization of hematopoietic stem and progenitor cells (HSPCs) from the bone marrow (BM) into the peripheral blood is a complex process that is enhanced dramatically under stress-induced conditions. A better understanding of how the mobilization process is regulated will likely facilitate the development of improved clinical protocols for stem cell harvesting and transplantation. In this issue of the JCI, Singh et al. (1) showed that the truncated cleaved form of neurotransmitter neuropeptide Y (NPY) actively promotes a breach of BM vascular sinusoidal portals, thereby augmenting HSPC trafficking to the circulation...
December 1, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28712386/neuropeptide-y-improves-cisplatin-induced-bone-marrow-dysfunction-without-blocking-chemotherapeutic-efficacy-in-a-cancer-mouse-model
#6
Min Hee Park, In Kyung Jung, Woo-Kie Min, Jin Ho Choi, Gyu Man Kim, Hee Kyung Jin, Jae-Sung Bae
Cisplatin is the most effective and widely used chemotherapeutic agent for many types of cancer. Unfortunately, its clinical use is limited by its adverse effects, notably bone marrow suppression leading to abnormal hematopoiesis. We previously revealed that neuropeptide Y (NPY) is responsible for the maintenance of hematopoietic stem cell (HSC) function by protecting the sympathetic nervous system (SNS) fibers survival from chemotherapy-induced bone marrow impairment. Here, we show the NPY-mediated protective effect against bone marrow dysfunction due to cisplatin in an ovarian cancer mouse model...
August 2017: BMB Reports
https://www.readbyqxmd.com/read/28656295/inhibition-of-neuropeptide-y-y1-receptor-induces-osteoblast-differentiation-in-mc3t3%C3%A2-e1-cells
#7
Motoki Yahara, Kanchu Tei, Masato Tamura
Neuropeptide Y (NPY) is a major neural signaling molecule. NPY is produced by peripheral tissues, such as osteoblasts, and binds to the corresponding Y1 receptor that belongs to the G‑protein‑coupled receptor family. Osteoblast‑specific Y1 receptor knockout mice exhibit high bone mass, indicating a role of the NPY‑Y1 receptor axis in the regulation of bone homeostasis. In the bone microenvironment, peripheral nerve fibers and osteoblasts produce NPY. However, the effects of the Y1 receptor on osteoblasts remain unexplored...
September 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28411439/neuropeptide-y-enhances-proliferation-and-prevents-apoptosis-in-rat-bone-marrow-stromal-cells-in-association-with-activation-of-the-wnt-%C3%AE-catenin-pathway-in-vitro
#8
Jianqun Wu, Song Liu, Huan Meng, Tianyu Qu, Su Fu, Zhao Wang, Jianguo Yang, Dan Jin, Bin Yu
Neuropeptide Y (NPY) exhibits a critical but poorly understood regulatory signaling function and has been shown to promote proliferation, vascularization and migration in several types of cells and tissues. However, little is known about the specific role of NPY in the proliferation and apoptosis of bone marrow stromal cells (also known as bone marrow-derived mesenchymal stem cells, BMSCs), which contain a subpopulation of multipotent skeletal stem cells. Based on BrdU incorporation tests, Cell Counting Kit-8, flow cytometry, quantitative polymerase chain reaction and western blotting, we showed that NPY significantly promoted the proliferation of BMSCs in a concentration-dependent manner, with a maximal effect observed at a concentration of 10(-10)M for pro-proliferative and 10(-12)M for anti-apoptotic activities...
May 2017: Stem Cell Research
https://www.readbyqxmd.com/read/28009825/neuropeptide-y1-receptor-regulates-glucocorticoid-induced-inhibition-of-osteoblast-differentiation-in-murine-mc3t3-e1-cells-via-erk-signaling
#9
Wei Yu, Chao Zhu, Wenning Xu, Leisheng Jiang, Shengdan Jiang
High dose glucocorticoid (GC) administration impairs the viability and function of osteoblasts, thus causing osteoporosis and osteonecrosis. Neuropeptide Y1 receptor (Y1 receptor) is expressed in bone tissues and cells, and regulates bone remodeling. However, the role of Y1 receptor in glucocorticoid-induced inhibition of osteoblast differentiation remains unknown. In the present study, osteoblastic cell line MC3T3-E1 cultured in osteogenic differentiation medium was treated with or without of 10(-7) M dexamethasone (Dex), Y1 receptor shRNA interference, Y1 receptor agonist [Leu(31), Pro(34)]-NPY, and antagonist BIBP3226...
December 21, 2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/27998395/neuropeptide-y-based-recombinant-peptides-ameliorate-bone-loss-in-mice-by-regulating-hematopoietic-stem-progenitor-cell-mobilization
#10
Min Hee Park, Namoh Kim, Hee Kyung Jin, Jae-Sung Bae
Ovariectomy-induced bone loss is related to an increased deposition of osteoclasts on bone surfaces. We reported that the 36-amino-acid-long neuropeptide Y (NPY) could mobilize hematopoietic stem/progenitor cells (HSPCs) from the bone marrow to the peripheral blood by regulating HSPC maintenance factors and that mobilization of HSPCs ameliorated low bone density in an ovariectomy-induced osteoporosis mouse model by reducing the number of osteoclasts. Here, we demonstrated that new NPY peptides, recombined from the cleavage of the full-length NPY, showed better functionality for HSPC mobilization than the full-length peptide...
March 2017: BMB Reports
https://www.readbyqxmd.com/read/27823858/ambient-temperature-modulates-the-effects-of-the-prader-willi-syndrome-candidate-gene-snord116-on-energy-homeostasis
#11
Y Qi, L Purtell, M Fu, K Sengmany, K Loh, L Zhang, S Zolotukhin, A Sainsbury, L Campbell, H Herzog
Germline deletion of the Prader-Willi syndrome (PWS) candidate gene Snord116 in mice leads to some classical symptoms of human PWS, notably reductions in body weight, linear growth and bone mass. However, Snord116 deficient mice (Snord116(-/-)) do not develop an obese phenotype despite their increased food intake and the underlying mechanism for that is unknown. We tested the phenotypes of germline Snord116(-/-) as well as neuropeptide Y (NPY) neuron specific Snord116(lox/lox)/NPY(cre/+) mice at 30°C, the thermoneutral temperature of mice, and compared these to previous reports studies conducted at normal room temperature...
February 2017: Neuropeptides
https://www.readbyqxmd.com/read/27802308/bone-injury-and-repair-trigger-central-and-peripheral-npy-neuronal-pathways
#12
Cecília J Alves, Inês S Alencastre, Estrela Neto, João Ribas, Sofia Ferreira, Daniel M Vasconcelos, Daniela M Sousa, Teresa Summavielle, Meriem Lamghari
Bone repair is a specialized type of wound repair controlled by complex multi-factorial events. The nervous system is recognized as one of the key regulators of bone mass, thereby suggesting a role for neuronal pathways in bone homeostasis. However, in the context of bone injury and repair, little is known on the interplay between the nervous system and bone. Here, we addressed the neuropeptide Y (NPY) neuronal arm during the initial stages of bone repair encompassing the inflammatory response and ossification phases in femoral-defect mouse model...
2016: PloS One
https://www.readbyqxmd.com/read/27720230/neuropeptide-y-accelerates-post-fracture-bone-healing-by-promoting-osteogenesis-of-mesenchymal-stem-cells
#13
Xiao-Chuan Gu, Xiao-Bin Zhang, Bing Hu, Ying Zi, Ming Li
Fracture repair is a complex yet well orchestrated regenerative process involving numerous signaling and cell types including osteoblasts. Here we showed that NPY, a neurotransmitter with regulatory functions in bone homeostasis, may contribute to the post-fracture bone healing in patients with traumatic brain injury-fracture combined injuries. Our results suggested NPY levels were increased in patients with the combined injuries, accomplished by arising of bone healing markers, such as ALP, OC, PICP and ICTP, than in those with simple fractures, and NPY have direct actions on MSCs to promote their osteogenic differentiation...
December 2016: Neuropeptides
https://www.readbyqxmd.com/read/27501818/the-central-nervous-system-and-bone-metabolism-an-evolving-story
#14
REVIEW
Paul Dimitri, Cliff Rosen
Our understanding of the control of skeletal metabolism has undergone a dynamic shift in the last two decades, primarily driven by our understanding of energy metabolism. Evidence demonstrating that leptin not only influences bone cells directly, but that it also plays a pivotal role in controlling bone mass centrally, opened up an investigative process that has changed the way in which skeletal metabolism is now perceived. Other central regulators of bone metabolism have since been identified including neuropeptide Y (NPY), serotonin, endocannabinoids, cocaine- and amphetamine-regulated transcript (CART), adiponectin, melatonin and neuromedin U, controlling osteoblast and osteoclast differentiation, proliferation and function...
May 2017: Calcified Tissue International
https://www.readbyqxmd.com/read/27090492/neuropeptide-y-induces-hematopoietic-stem-progenitor-cell-mobilization-by-regulating-matrix-metalloproteinase-9-activity-through-y1-receptor-in-osteoblasts
#15
Min Hee Park, Jong Kil Lee, Namoh Kim, Woo-Kie Min, Jeong Eun Lee, Kyoung-Tae Kim, Haruhiko Akiyama, Herbert Herzog, Edward H Schuchman, Hee Kyung Jin, Jae-Sung Bae
Hematopoietic stem/progenitor cell (HSPC) mobilization is an essential homeostatic process regulated by the interaction of cellular and molecular components in bone marrow niches. It has been shown by others that neurotransmitters released from the sympathetic nervous system regulate HSPC egress from bone marrow to peripheral blood. In this study, we investigate the functional role of neuropeptide Y (NPY) on this process. NPY deficient mice had significantly impaired HSPC mobilization due to increased expression of HSPC maintenance factors by reduction of matrix metalloproteinase-9 (MMP-9) activity in bone marrow...
August 2016: Stem Cells
https://www.readbyqxmd.com/read/27080706/neuropeptide-y-mediates-glucocorticoid-induced-osteoporosis-and-marrow-adiposity-in-mice
#16
F-S Wang, W-S Lian, W-T Weng, Y-C Sun, H-J Ke, Y-S Chen, J-Y Ko
UNLABELLED: Increased neuropeptide Y (NPY) expression occurred in the glucocorticoid-induced osteoporotic skeleton. NPY knockout mice exhibited a minor response to the glucocorticoid-mediated exacerbation of bone accretion and fatty marrow pathogenesis. NPY deletion restored SITR1 signaling and enhanced PPARγ ubiquitination of bone tissue, an alternative strategy for ameliorating glucocorticoid-induced skeletal deterioration. INTRODUCTION: Glucocorticoid excess is observed to worsen the pathogenesis of osteoporosis and fatty marrow...
September 2016: Osteoporosis International
https://www.readbyqxmd.com/read/26872458/osteoblastic-actions-of-the-neuropeptide-y-system-to-regulate-bone-and-energy-homeostasis
#17
REVIEW
Harry Horsnell, Paul A Baldock
Neural pathways are now a well-appreciated factor in the regulatory milieu controlling the maintenance of bone mass. A number of neural pathways from the brain to bone have been identified. These pathways often involve elements of the energy homeostatic apparatus, indicating links between the regulation of bone metabolism and energy balance. Neuropeptide Y is one such factor that co-regulates these two processes. Initial studies outlined the skeletal actions of NPY from within the brain and the interactions with energy homeostatic processes...
February 2016: Current Osteoporosis Reports
https://www.readbyqxmd.com/read/26824232/prader-willi-critical-region-a-non-translated-imprinted-central-regulator-of-bone-mass-possible-role-in-skeletal-abnormalities-in-prader-willi-syndrome
#18
Ee-Cheng Khor, Bruce Fanshawe, Yue Qi, Sergei Zolotukhin, Rishikesh N Kulkarni, Ronaldo F Enriquez, Louise Purtell, Nicola J Lee, Natalie K Wee, Peter I Croucher, Lesley Campbell, Herbert Herzog, Paul A Baldock
Prader-Willi Syndrome (PWS), a maternally imprinted disorder and leading cause of obesity, is characterised by insatiable appetite, poor muscle development, cognitive impairment, endocrine disturbance, short stature and osteoporosis. A number of causative loci have been located within the imprinted Prader-Willi Critical Region (PWCR), including a set of small non-translated nucleolar RNA's (snoRNA). Recently, micro-deletions in humans identified the snoRNA Snord116 as a critical contributor to the development of PWS exhibiting many of the classical symptoms of PWS...
2016: PloS One
https://www.readbyqxmd.com/read/26728272/neuropeptide-y-protects-kidney-against-cisplatin-induced-nephrotoxicity-by-regulating-p53-dependent-apoptosis-pathway
#19
Namoh Kim, Woo-Kie Min, Min Hee Park, Jong Kil Lee, Hee Kyung Jin, Jae-Sung Bae
Cisplatin is a platinum-based chemotherapeutic drug for treating various types of cancers. However, the use of cisplatin is limited by its negative effect on normal tissues, particularly nephrotoxicity. Various mechanisms such as DNA adduct formation, mitochondrial dysfunction, oxidative stress, and apoptosis are involved in the adverse effect induced by cisplatin treatment. Several studies have suggested that neuropeptide Y (NPY) is involved in neuroprotection as well as restoration of bone marrow dysfunction from chemotherapy induced nerve injury...
May 2016: BMB Reports
https://www.readbyqxmd.com/read/26707636/neuropeptide-y-stimulates-osteoblastic-differentiation-and-vegf-expression-of-bone-marrow-mesenchymal-stem-cells-related-to-canonical-wnt-signaling-activating-in-vitro
#20
Song Liu, Dan Jin, Jian-qun Wu, Zi-yi Xu, Su Fu, Gang Mei, Zhen-Lv Zou, Sheng-hui Ma
Neuropeptide Y (NPY) is a neuropeptide secreted by sensory nerve fibers distributed in the marrow and vascular canals of bone tissue. However, the effect of NPY on the osteogenic ability of bone marrow mesenchymal stem cells (BMSCs) remains controversial and has not been thoroughly investigated. To explore the osteogenic activity and the migration and VEGF expression capabilities of BMSCs affected by NPY, as well as the underlying mechanisms, we investigated the potential relationships among NPY, osteoblastic differentiation, angiogenesis and canonical Wnt signaling in BMSCs...
April 2016: Neuropeptides
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