



@article {2843,
	title = {Neuropeptide y modulates fracture healing through Y1 receptor signaling},
	journal = {Journal of Orthopaedic Research},
	volume = {31},
	year = {2013},
	note = {Export Date: 12 December 2013Source: Scopus},
	month = {2013///},
	pages = {1570 - 1578},
	url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84882886747\&partnerID=40\&md5=dd7576a200a42ce37ff5a98115fe9462},
	author = {Sousa, D.M. and McDonald, M.M. and Mikulec, K. and Peacock, L. and Herzog, H. and Lamghari, M. and Little, D.G. and Baldock, P.A.}
}
@article {2204,
	title = {Neuropeptide Y Y1 receptor antagonism increases bone mass in mice},
	journal = {BoneBone},
	volume = {51},
	year = {2012},
	note = {Export Date: 21 November 2012Source: ScopusCODEN: BONEDdoi: 10.1016/j.bone.2012.03.020PubMed ID: 22484690Language of Original Document: EnglishCorrespondence Address: Herzog, H.; Neuroscience Research Program, Garvan Institute of Medical Research, 384 Victoria St, Darlinghurst, Sydney, NSW 2010, Australia; email: h.herzog@garvan.org.auChemicals/CAS: corticosterone, 50-22-6; glucose, 50-99-7, 84778-64-3; n2 diphenylacetyl n (4 ureidomethylbenzyl)argininamide, 191868-14-1, 217977-06-5; neuropeptide Y, 82785-45-3, 83589-17-7; Arginine, 74-79-3; BIBO 3304; Glucose, 50-99-7; Receptors, Neuropeptide Y; neuropeptide Y-Y1 receptorTradenames: bibo 3304References: Karaguzel, G., Holick, M.F., Diagnosis and treatment of osteopenia (2010) Rev Endocr Metab Disord, 11, pp. 237-251;Burge, R., Dawson-Hughes, B., Solomon, D.H., Wong, J.B., King, A., Tosteson, A., Incidence and economic burden of osteoporosis-related fractures in the United States, 2005-2025 (2007) J Bone Miner Res, 22, pp. 465-475; 
Nguyen, N.D., Ahlborg, H.G., Center, J.R., Eisman, J.A., Nguyen, T.V., Residual lifetime risk of fractures in women and men (2007) J Bone Miner Res, 22, pp. 781-788; 
Goltzman, D., Discoveries, drugs and skeletal disorders (2002) Nat Rev Drug Discov, 1, pp. 784-796; 
Jorgensen, N.R., Schwarz, P., Effects of anti-osteoporosis medications on fracture healing (2011) Curr Osteoporos Rep, 9, pp. 149-155; 
Elefteriou, F., Regulation of bone remodeling by the central and peripheral nervous system (2008) Arch Biochem Biophys, 473, pp. 231-236; 
Teixeira, L., Sousa, D.M., Nunes, A.F., Sousa, M.M., Herzog, H., Lamghari, M., NPY revealed as a critical modulator of osteoblast function in vitro: new insights into the role of Y1 and Y2 receptors (2009) J Cell Biochem, 107, pp. 908-916; 
Lee, N.J., Doyle, K.L., Sainsbury, A., Enriquez, R.F., Hort, Y.J., Riepler, S.J., Critical role for Y1 receptors in mesenchymal progenitor cell differentiation and osteoblast activity (2010) J Bone Miner Res, 25, pp. 1736-1747; 
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Zhang, L., Macia, L., Turner, N., Enriquez, R.F., Riepler, S.J., Nguyen, A.D., Peripheral neuropeptide Y Y1 receptors regulate lipid oxidation and fat accretion (2010) Int J Obes (Lond), 34, pp. 357-373; 
Painsipp, E., Sperk, G., Herzog, H., Holzer, P., Delayed stress-induced differences in locomotor and depression-related behaviour in female neuropeptide-Y Y1 receptor knockout mice (2010) J Psychopharmacol, 24, pp. 1541-1549; 
Movafagh, S., Hobson, J.P., Spiegel, S., Kleinman, H.K., Zukowska, Z., Neuropeptide Y induces migration, proliferation, and tube formation of endothelial cells bimodally via Y1, Y2, and Y5 receptors (2006) FASEB J, 20, pp. 1924-1926; 
Hansel, D.E., Eipper, B.A., Ronnett, G.V., Neuropeptide Y functions as a neuroproliferative factor (2001) Nature, 410, pp. 940-944; 
Baldock, P.A., Allison, S.J., Lundberg, P., Lee, N.J., Slack, K., Lin, E.-J.D., Novel role of Y1 receptors in the coordinated regulation of bone and energy homeostasis (2007) J Biol Chem, 282, pp. 19092-19102; 
Lee, N.J., Nguyen, A.D., Enriquez, R.F., Doyle, K.L., Sainsbury, A., Baldock, P.A., Osteoblast specific Y1 receptor deletion enhances bone mass (2011) Bone, 48, pp. 461-467; 
Lundberg, P., Allison, S.J., Lee, N.J., Baldock, P.A., Brouard, N., Rost, S., Greater bone formation of Y2 knockout mice is associated with increased osteoprogenitor numbers and altered Y1 receptor expression (2007) J Biol Chem, 282, pp. 19082-19091; 
Igwe, J.C., Jiang, X., Paic, F., Ma, L., Adams, D.J., Baldock, P.A., Neuropeptide Y is expressed by osteocytes and can inhibit osteoblastic activity (2009) J Cell Biochem, 108, pp. 621-630; 
Zhang, L., Bijker, M.S., Herzog, H., The neuropeptide Y system: pathophysiological and therapeutic implications in obesity and cancer (2011) Pharmacol Ther, 131, pp. 91-113; 
Yulyaningsih, E., Zhang, L., Herzog, H., Sainsbury, A., NPY receptors as potential targets for anti-obesity drug development (2011) Br J Pharmacol, 163, pp. 1170-1202; 
Wieland, H.A., Engel, W., Eberlein, W., Rudolf, K., Doods, H.N., Subtype selectivity of the novel nonpeptide neuropeptide Y Y1 receptor antagonist BIBO 3304 and its effect on feeding in rodents (1998) Br J Pharmacol, 125, pp. 549-555; 
Polidori, C., Ciccocioppo, R., Regoli, D., Massi, M., Neuropeptide Y receptor(s) mediating feeding in the rat: characterization with antagonists (2000) Peptides, 21, pp. 29-35; 
Dailey, M.J., Bartness, T.J., Appetitive and consummatory ingestive behaviors stimulated by PVH and perifornical area NPY injections (2009) Am J Physiol Regul Integr Comp Physiol, 296, pp. R877-R892; 
Zhang, L., Lee, N.J., Nguyen, A.D., Enriquez, R.F., Riepler, S.J., Stehrer, B., Additive actions of the cannabinoid and neuropeptide Y systems on adiposity and lipid oxidation (2010) Diabetes Obes Metab, 12, pp. 591-603; 
Matsuda, H., Brumovsky, P.R., Kopp, J., Pedrazzini, T., Hokfelt, T., Distribution of neuropeptide Y Y1 receptors in rodent peripheral tissues (2002) J Comp Neurol, 449, pp. 390-404; 
Baldock, P.A., Sainsbury, A., Allison, S., Lin, E.-J.D., Couzens, M., Boey, D., Hypothalamic control of bone formation: distinct actions of leptin and Y2 receptor pathways (2005) J Bone Miner Res, 20, pp. 1851-1857; 
Kushi, A., Sasai, H., Koizumi, H., Takeda, N., Yokoyama, M., Nakamura, M., Obesity and mild hyperinsulinemia found in neuropeptide Y-Y1 receptor-deficient mice (1998) Proc Natl Acad Sci U S A, 95, pp. 15659-15664; 
Kempna, P., Korner, M., Waser, B., Hofer, G., Nuoffer, J.M., Reubi, J.C., Neuropeptide Y modulates steroid production of human adrenal H295R cells through Y1 receptors (2010) Mol Cell Endocrinol, 314, pp. 101-109; 
Burcelin, R., Brunner, H., Seydoux, J., Thorensa, B., Pedrazzini, T., Increased insulin concentrations and glucose storage in neuropeptide Y Y1 receptor-deficient mice (2001) Peptides, 22, pp. 421-427; 
Buckwalter, J.A., Cooper, R.R., Bone structure and function (1987) Instr Course Lect, 36, pp. 27-48; 
El-Sherif, N., Turitto, G., Electrolyte disorders and arrhythmogenesis (2011) Cardiol J, 18, pp. 233-245; 
Amano, S., Arai, M., Goto, S., Togari, A., Inhibitory effect of NPY on isoprenaline-induced osteoclastogenesis in mouse bone marrow cells (2007) Biochim Biophys Acta, 1770, pp. 966-973; 
Wheway, J., Mackay, C.R., Newton, R.A., Sainsbury, A., Boey, D., Herzog, H., A fundamental bimodal role for neuropeptide Y1 receptor in the immune system (2005) J Exp Med, 202, pp. 1527-1538; 
Datta, H.K., Ng, W.F., Walker, J.A., Tuck, S.P., Varanasi, S.S., The cell biology of bone metabolism (2008) J Clin Pathol, 61, pp. 577-587; 
Bedoui, S., Kawamura, N., Straub, R.H., Pabst, R., Yamamura, T., von H{\"o}rsten, S., Relevance of neuropeptide Y for the neuroimmune crosstalk (2003) J Neuroimmunol, 134, pp. 1-11; 
Allison, S.J., Baldock, P.A., Enriquez, R.F., Lin, E., During, M., Gardiner, E.M., Critical interplay between neuropeptide Y and sex steroid pathways in bone and adipose tissue homeostasis (2009) J Bone Miner Res, 24, pp. 294-304; 
Frolik, C.A., Black, E.C., Cain, R.L., Satterwhite, J.H., Brown-Augsburger, P.L., Sato, M., Anabolic and catabolic bone effects of human parathyroid hormone (1-34) are predicted by duration of hormone exposure (2003) Bone, 33, pp. 372-379; 
Vahle, J.L., Long, G.G., Sandusky, G., Westmore, M., Ma, Y.L., Sato, M., Bone neoplasms in F344 rats given teriparatide [rhPTH(1-34)] are dependent on duration of treatment and dose (2004) Toxicol Pathol, 32, pp. 426-438
},
	month = {2012///},
	pages = {8 - 16},
	abstract = {The neuropeptide Y system has emerged as one of the major neural signalling pathways regulating bone homeostasis. Absence of Y1 receptor signalling from bone forming osteoblasts is responsible for an enhancement on bone mass in mice, suggesting that pharmacological blockade of Y1 receptors may offer a novel anabolic treatment option for improving bone mass. Here we show that oral administration of the selective Y1 receptor antagonist BIBO3304 for 8. weeks dose-dependently increases bone mass in mice. Histomorphometric analysis revealed a significant 1.5-fold increase in cancellous bone volume in the femora of mice treated with BIBO3304. Furthermore, bone microarchitecture was improved, with greater trabecular number and trabecular thickness. This increase in bone mass was associated with a significant increase in bone anabolic activity of osteoblasts and, interestingly, was evident despite a coincident increase in bone resorption, as evidenced by an increase in the number of the osteolytic osteoclasts. Changes were also evident in cortical bone, with a significant increase in periosteal mineral apposition rate. Importantly, no adverse extra-skeletal side effects were observed through Y1 receptor antagonism over the 8-week treatment period, with no effects of even the higher BIBO3304 dose on body weight, adiposity, energy metabolism or circulating corticosterone levels. Taken together, this work describes the first NPY-based anabolic treatment for improving bone mass, and highlights the therapeutic potential of blocking Y1 receptor signalling for the prevention of, or recovery from, degenerative skeletal diseases. {\textcopyright} 2012 Elsevier Inc.},
	keywords = {animal experiment, animal tissue, Animals, Arginine, article, body weight, Bone Density, bone mass, bone metabolism, bone strength, cancellous bone, controlled study, cortical bone, corticosterone, corticosterone blood level, dose response, Dose-Response Relationship, Drug, drug effect, drug mechanism, drug megadose, energy metabolism, femur, food intake, glucose, glucose homeostasis, Homeostasis, male, Mice, Mice, Inbred C57BL, morphometrics, mouse, n2 diphenylacetyl n (4 ureidomethylbenzyl)argininamide, neuropeptide Y, Neuropeptide yY, nonhuman, obesity, Oral drug administration, osteoblast, osteoclast activity, Osteogenesis, osteolysis, Osteopenia, Receptors, Neuropeptide Y, signal transduction, trabecular bone, Y1 receptor antagonism},
	isbn = {87563282 (ISSN)},
	url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84859915620\&partnerID=40\&md5=29596d34bad3cbf751d1cbfadb63abb9},
	author = {Sousa, D.M. and Baldock, P.A. and Enriquez, R.F. and Zhang, L. and Sainsbury, A. and Lamghari, M. and Herzog, H.}
}
@article {2303,
	title = {NPY revealed as a critical modulator of osteoblast function in vitro: New insights into the role of Y1 and Y2 receptors},
	journal = {Journal of Cellular BiochemistryJ. Cell. Biochem.},
	volume = {107},
	year = {2009},
	note = {Cited By (since 1996): 12Export Date: 21 November 2012Source: ScopusCODEN: JCEBDdoi: 10.1002/jcb.22194PubMed ID: 19459152Language of Original Document: EnglishCorrespondence Address: Lamghari, M.; Instituto de Engenharia Biom{\'e}dica (INEB), Divis{\~a}o de Biomateriais, Universidade do Porto, Rua do Campo Alegre, 823, 4150-180 Porto, Portugal; email: lamghari@ineb.up.ptChemicals/CAS: calcium, 14092-94-5, 7440-70-2; osteoclast differentiation factor, 200145-93-3; osteoprotegerin, 205944-50-9; Alkaline Phosphatase, 3.1.3.1; Neuropeptide Y; Osteoprotegerin; RANK Ligand; Receptors, Neuropeptide YReferences: Ahmed, M., Srinivasan, G.R., Theodorsson, E., Bjurholm, A., Kreicbergs, A., Extraction and quantitation of neuropeptides in bone by radioimmunoassay (1994) Regul Pept, 51, pp. 179-188;Allison, S.J., Herzog, H., NPY and bone (2006) EXS, 95, pp. 171-182; 
Allison, S.J., Baldock, P., Sainsbury, A., Enriquez, R., Lee, N.J., Lin, E.J., Klugman, M., Gardiner, E.M., Conditional deletion of hypothalamic Y2 receptors reverts gonadectomy-induced bone loss in adult mice (2006) J Biol Chem, 281, pp. 23436-23444; 
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Baldock, P.A., Sainsbury, A., Couzens, M., Enriquez, R.F., Ghomas, G.P., Gardiner, E.M., Herzog, H., Hypothalamic Y2 receptors regulate bone formation (2002) J Clin Investig, 109, pp. 915-921; 
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Wittmann, W., Loacker, S., Kapeller, I., Herzog, H., Schwarzer, C., Y1-receptors regulate the expression of Y2-receptors in distinct mouse forebrain areas (2005) Neuroscience, 136, pp. 241-250; 
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},
	month = {2009///},
	pages = {908 - 916},
	abstract = {Neuropeptide Y (NPY) has recently emerged as a potential regulator of bone homeostasis. However, the relevance of NPY{\textquoteright}s role in osteoblast activity and the biological functions involving NPY receptors in bone homeostasis remain to be clarified. Here we report that chronically elevated NPY levels leaded to a modulation of the level of Y2 receptor expression marked with a transient down and upregulation according to the stage of osteoblast differentiation. We also show that NPY is a negative regulator of Y1 receptor expression. The pharmalogical activation of Y2 receptor with its agonist resulted in similar effect. Functional analysis also revealed the osteogenic potential of NPY with osteoblast phenotype markers being significantly enhanced in osteoprogenitor cells stimulated by NPY, probably due to the down-regulation of Y1 receptor. In contrasts, these cells exhibit a reduction in calcium deposition in extracellular matrix most likely mediated via Y2 receptor signalling. Furthermore, we show that NPY modulates receptor activator of nuclear factor kB (NF-kB) (RANK) ligand and osteoprotegerin, two key factors regulating bone remodelling. Specifically, NPY inhibits the transcriptional activity of RANKL promoter in osteoprogenitor cells and enhances OPG expression in osteoblasts at early stages of differentiation. However, NPY effect on OPG seemed to be unrelated to Y2 receptor activation. Taken together the present data supported the contribution of NPY pathway in bone homeostasis via a direct action on osteoblasts cells. {\textcopyright} 2009 Wiley-Liss, Inc.},
	keywords = {alkaline phosphatase, animal cell, animal tissue, Animals, article, Bone, Bone Marrow Cells, bone remodeling, Calcium, cell activity, cell differentiation, cell function, Cell Line, cell stimulation, controlled study, down regulation, extracellular matrix, gene expression regulation, genetic transcription, Homeostasis, immunoglobulin enhancer binding protein, in vitro study, Mice, neuropeptide Y, neuropeptide Y1 receptor, neuropeptide Y2 receptor, nonhuman, NPY, nuclear factor Y, osteoblast, Osteoblasts, osteoclast differentiation factor, Osteoprotegerin, phenotype, priority journal, promoter region, protein expression, RANK Ligand, Receptors, Neuropeptide Y, Reverse Transcriptase Polymerase Chain Reaction, signal transduction, stem cell, Stromal Cells, upregulation, Y1 receptor, Y2 receptor},
	isbn = {07302312 (ISSN)},
	url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-67749108153\&partnerID=40\&md5=3fac97e90b88592291766e499000ae54},
	author = {Teixeira, L. and Sousa, D.M. and Nunes, A.F. and Sousa, M.M. and Herzog, H. and Lamghari, M.}
}
@article {2311,
	title = {NPY signalling pathway in bone homeostasis: Y1 receptor as a potential drug target},
	journal = {Current Drug TargetsCurr. Drug Targets},
	volume = {10},
	year = {2009},
	note = {Cited By (since 1996): 5Export Date: 21 November 2012Source: ScopusCODEN: CDTUAdoi: 10.2174/138945009787122888Language of Original Document: EnglishCorrespondence Address: Lamghari, M.; INEB - Instituto de Engenharia Biom{\'e}dica, Universidade do Porto, NEWTherapies Group, Rua do Campo Alegre 823, 4150-180 Porto, Portugal; email: lamghari@ineb.up.ptChemicals/CAS: gr 231118, 158859-98-4; n [1 [4 [[[[4 [(dimethylamino)methyl]cyclohexyl]methyl]amino]iminomethyl]benzyl] 2 oxo 2 (1 pyrrolidinyl)ethyl] alpha [(2 naphthalenylsulfonyl)amino]benzenepropanamide, 163238-19-5; n2 diphenylacetyl n (4 ureidomethylbenzyl)argininamide, 191868-14-1, 217977-06-5; nalpha (diphenylacetyl) n (4 hydroxybenzyl) dextro argininamide, 159013-54-4; neuropeptide Y, 82785-45-3, 83589-17-7; peptide YY, 81858-94-8; Ligands; Neuropeptide Y; Receptors, Neuropeptide YTradenames: bibo 3304; bibp 3226; gi 264879a; gr 231118; gw 1229; j 115814; ly 357897; sr 120819aReferences: Lundberg, P., Lerner, U.H., (2002) Microsc. Res. Tech, 58 (2), pp. 98-103;Baldock, P.A., Sainsbury, A., Couzens, M., Enriquez, R.F., Thomas, G.P., Gardiner, E.M., Herzog, H., (2002) J. Clin. Invest, 109 (7), pp. 915-921; 
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},
	month = {2009///},
	pages = {9 - 19},
	abstract = {Neuropeptide (NPY) is a neurotransmitter widely distributed in central and peripheral nervous system that has been implicated in several physiological processes through activation of five different Y receptors: Y1, Y2, Y4, Y5, and y6. NPY system has been extensively studied for the last decades due to its implications in a wide variety of physiological processes. For this purpose a diversity of sophisticated animal models and receptors agonists and antagonists has been developed to better understand its actions throughout body homeostasis. Consequently, NPY and its receptors have recently emerged as a potential regulator of bone homeostasis. This is supported by the demonstration of an increase of bone mass in mice lacking Y1 or Y2 receptor genes. Recent findings revealed Y1 receptor as a potential drug target candidate for prevention and treatment of bone loss. Indeed, it has been demonstrated that osteoblasts express Y1 receptor while no other Y receptor was detected in these cells, implicating Y1 receptor signalling in the local control of bone turnover. In this review, we have summarized the findings obtained from studies on NPY system in skeletogenesis focusing on Y1 receptor. {\textcopyright} 2009 Bentham Science Publishers Ltd.},
	keywords = {1 [1 [3 [(3 piperidyl)]]propyl] 2 [[(4 chlorophenoxyl)methyl]indol 3 yl] 2 (4 piperidylpiperidyl)ethan 1 one, 2 [1 (3 chloro 5 isopropoxycarbonylaminophenyl)ethylamino] 6 [2 (5 ethyl 4 methyl 2 thiazolyl)ethyl] 4 morpholinopyridine, 2 [1 (3 chloro 5 isopropyloxycarbonylaminophenyl)ethylamino] 6 [2 (5 ethyl 4 methyl 1,3 thiazol 2 yl)ethyl] 4 morpholinopyridine, Amino Acid Sequence, animal, Animals, bone development, bone mass, bone remodeling, Bone remodelling, bone turnover, Brain, drug antagonism, drug effect, drug potentiation, drug targeting, genetics, gi 264879a, gr 231118, Homeostasis, human, Humans, ligand, Ligands, ly 357897, metabolism, molecular genetics, Molecular Sequence Data, n alpha [3,3 bis(1 naphthyl)propionyl]dextro arginine n [1 benzyl 2 methoxyethyl]amide, n [1 [4 [[[[4 [(dimethylamino)methyl]cyclohexyl]methyl]amino]iminomethyl]benzyl] 2 oxo 2 (1 pyrrolidinyl)ethyl] alpha [(2 naphthalenylsulfonyl)amino]benzenepropanamide, n2 diphenylacetyl n (4 ureidomethylbenzyl)argininamide, nalpha (diphenylacetyl) n (4 hydroxybenzyl) dextro argininamide, neuropeptide Y, neuropeptide Y receptor, neuropeptide Y receptor agonist, neuropeptide Y receptor antagonist, neuropeptide Y [25 dextro arginine], neuropeptide Y [26 dextro histidine], neuropeptide Y [31 leucine 34 proline], neuropeptide Y [6 arginine 34 proline], neuropeptide Y [7 phenylalanine 34 proline], neuropeptide Y1 receptor, neuropeptide Y2 receptor, neuropeptide Y4 receptor, neuropeptide Y5 receptor, neuropeptide Y6 receptor, nonhuman, osteoblast, osteoclast, osteolysis, peptide YY, peptide YY [31 leucine 34 proline], peptide YY [34 proline], pharmacological blocking, physiology, protein binding, protein expression, protein family, protein isolation, receptor intrinsic activity, Receptors, Neuropeptide Y, review, signal transduction, unclassified drug, Y1 receptor},
	isbn = {13894501 (ISSN)},
	url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-63049117952\&partnerID=40\&md5=2e70b182cba78971a24c5a8124b7799b},
	author = {Sousa, D.M. and Herzog, H. and Lamghari, M.}
}
