The role of Wnt signaling pathway during central nervous system development and diseases

Abstract

Abstract: Wnt signaling pathway that widely exists in multicellular eukaryotes and plays an essential, decisive and directional role in regulation of a variety of life processes is one highly conservative signaling pathway. Traumatic brain injury, cerebral stroke and neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD) that have a high rate of fatality and disability, are still the important diseases threatening the health of human beings around the world. In recent years, Wnt signaling pathway has gradually drawn more and more attention from people for the critical role played in neural development and central nervous system (CNS) diseases. To clarify the molecular mechanisms of Wnt signaling pathway comprehensively and deeply will probably offer new ideas and methods to the prevention and treatment of CNS diseases. This article summarizes the important role in regulating cellular development and demise and the relationship of canonical Wnt/β-catenin signaling pathway with the neurological diseases.

Key words: Wnt/β-catenin, β-catenin, GSK-3β, Neural development, CNS diseases

CLC Number:

R966

LIU Mei, LIAO Hong. The role of Wnt signaling pathway during central nervous system development and diseases[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2013, 18(9): 1059-1064.

References

[1] Klaus A, Birchmeier W. Wnt signalling and its impact on development and cancer[J]. Nat Rev Cancer, 2008, 8(5): 387-398.
[2] Wray J, Hartmann C. WNTing embryonic stem cells[J]. Trends Cell Biol, 2012, 22(3): 159-168.
[3] Verkaar F, Zaman GJ. New avenues to target Wnt/β-catenin signaling[J]. Drug Discov Today, 2011, 16(1/2): 35-41.
[4] Park M, Shen K. WNTs in synapse formation and neuronal circuitry[J]. EMBO J, 2012, 31(12): 2697-2704.
[5] 尹定子, 宋海云. Wnt信号通路:调控机理和生物学意义[J]. 中国细胞生物学学报, 2011, 33(2): 103-111.
[6] Komiya Y, Habas R. Wnt signal transduction pathways[J]. Organogenesis, 2008, 4(2): 68-75.
[7] Ille F, Atanasoski S, Falk S, et al. Wnt/BMP signal integration regulates the balance between proliferation and differentiation of neuroepithelial cells in the dorsal spinal cord[J]. Dev Biol, 2007, 304(1): 394-408.
[8] Hayward P, Kalmar T, Arias AM. Wnt/Notch signalling and information processing during development [J]. Development, 2008, 135(3): 411-424.
[9] Moon RT, Kohn AD, De Ferrari GV, et al. WNT and beta-catenin signalling: diseases and therapies[J]. Nat Rev Genet, 2004, 5(9): 691-701.
[10] Toledo EM, Colombres M, Inestrosa NC. Wnt signaling in neuroprotection and stem cell differentiation [J]. Prog Neurobiol, 2008, 86(3): 281-296.
[11] Zechner D, Fujita Y, Hülsken J, et al. beta-Catenin signals regulate cell growth and the balance between progenitor cell expansion and differentiation in the nervous system [J]. Dev Biol, 2003, 258(2): 406-418.
[12] McMahon AP, Bradley A. The Wnt-1 (int-1) proto-oncogene is required for development of a large region of the mouse brain[J]. Cell, 1990, 62(6): 1073-1085.
[13] Viti J, Gulacsi A, Lillien L. Wnt regulation of progenitor maturation in the cortex depends on Shh or fibroblast growth factor 2[J]. J Neurosci, 2003, 23(13): 5919-5927.
[14] Castelo-Branco G, Wagner J, Rodriguez FJ, et al. Differential regulation of midbrain dopaminergic neuron development by Wnt-1, Wnt-3a, and Wnt-5a[J]. Proc Natl Acad Sci USA, 2003, 100(22): 12747-12752.
[15] Hooper C, Markevich V, Plattner F, et al. Glycogen synthase kinase-3 inhibition is integral to long-term potentiation[J]. Eur J Neurosci, 2007, 25(1): 81-86.
[16] Lie DC, Colamarino SA, Song HJ, et al. Wnt signalling regulates adult hippocampal neurogenesis[J]. Nature, 2005, 437(7063): 1370-1375.
[17] Sebastião AM, Colino-Oliveira M, Assaife-Lopes N, et al. Lipid rafts, synaptic transmission and plasticity: impact in age-related neurodegenerative diseases[J]. Neuropharmacology, 2013, 64: 97-107.
[18] Ahmad-Annuar A, Ciani L, Simeonidis I, et al. Signaling across the synapse: a role for Wnt and Dishevelled in presynaptic assembly and neurotransmitter release[J]. J Cell Biol, 2006, 174(1): 127-139.
[19] Cerpa W, Godoy JA, Alfaro I, et al. Wnt-7a modulates the synaptic vesicle cycle and synaptic transmission in hippocampal neurons[J]. J Biol Chem, 2008, 283(9): 5918-5927.
[20] Rodriguez-Gil DJ, Hu W, Greer CA. Dishevelled proteins are associated with olfactory sensory neuron presynaptic terminals[J]. PLoS One, 2013, 8(2): e56561.
[21] Davis EK, Zou Y, Ghosh A. Wnts acting through canonical and noncanonical signaling pathways exert opposite effects on hippocampal synapse formation[J]. Neural Dev, 2008, 3:32. doi: 10.1186/1749- 8104-3-32.
[22] Chen J, Park CS, Tang SJ. Activity-dependent synaptic Wnt release regulates hippocampal long term potentiation[J]. J Biol Chem, 2006, 281(17): 11910-11916.
[23] Peineau S, Taghibiglou C, Bradley C, et al. LTP inhibits LTD in the hippocampus via regulation of GSK3β[J]. Neuron, 2007, 53(5): 703-717.
[24] Duchen MR. Mitochondria, calcium-dependent neuronal death and neurodegenerative disease[J]. Pflugers Arch, 2012, 464(1): 111-121.
[25] Zhao J, Kim KA, Abo A. Tipping the balance: modulating the Wnt pathway for tissue repair[J]. Trends Biotechnol, 2009, 27(3): 131-136.
[26] Chen S, Guttridge DC, You Z, et al. Wnt-1 signaling inhibits apoptosis by activating beta-catenin/T cell factor-mediated transcription[J]. J Cell Biol, 2001, 152(1): 87-96.
[27] Alvarez AR, Godoy JA, Mullendorff K, et al. Wnt-3a overcomes beta-amyloid toxicity in rat hippocampal neurons[J]. Exp Cell Res, 2004, 297(1): 186-196.
[28] Steinhusen U, Badock V, Bauer A, et al. Apoptosis-induced cleavage of beta-catenin by caspase-3 results in proteolytic fragments with reduced transactivation potential[J]. J Biol Chem, 2000, 275(21): 16345-16353.
[29] Hayashi-Takagi A, Barker PB, Sawa A. Readdressing synaptic pruning theory for schizophrenia: Combination of brain imaging and cell biology[J]. Commun Integr Biol, 2011, 4(2): 211-212.
[30] Singh KK. An emerging role for Wnt and GSK3 signaling pathways in schizophrenia[J]. Clin Genet, 2013, 83(6): 511-517.
[31] Sutton LP, Rushlow WJ. The effects of neuropsychiatric drugs on glycogen synthase kinase-3 signaling[J]. Neuroscience, 2011, 199: 116-124.
[32] 任红,廖红. 以淀粉样蛋白Aβ为靶点治疗阿尔茨海默病的研究进展[J]. 中国临床药理学与治疗学,2012, 17(10): 1172-1178.
[33] Magdesian MH, Carvalho MM, Mendes FA, et al. Amyloid-beta binds to the extracellular cysteine-rich domain of Frizzled and inhibits Wnt/beta-catenin signaling[J]. J Biol Chem, 2008, 283(14): 9359-9368.
[34] Hooper C, Killick R, Lovestone S. The GSK3 hypothesis of Alzheimer's disease[J]. J Neurochem, 2008, 104(6): 1433-1439.
[35] Caricasole A, Copani A, Caraci F, et al. Induction of Dickkopf-1, a negative modulator of the Wnt pathway, is associated with neuronal degeneration in Alzheimer's brain[J]. J Neurosci, 2004, 24(26): 6021-6027.
[36] Rosi MC, Luccarini I, Grossi C, et al. Increased Dickkopf-1 expression in transgenic mouse models of neurodegenerative disease[J]. J Neurochem, 2010, 112(6): 1539-1551.
[37] Cerpa W, Farías GG, Godoy JA, et al. Wnt-5a occludes Abeta oligomer-induced depression of glutamatergic transmission in hippocampal neurons[J]. Mol Neurodegener, 2010,5: 3. doi: 10.1186/ 1750-1326-5-3.
[38] Zhou Y, Luo Y, Dai J. Axonal and dendritic changes are associated with diabetic encephalopathy in rats: an important risk factor for Alzheimer's disease[J]. J Alzheimers Dis, 2013, 34(4): 937-947.
[39] West AB, Moore DJ, Choi C, et al. Parkinson's disease-associated mutations in LRRK2 link enhanced GTP-binding and kinase activities to neuronal toxicity[J]. Hum Mol Genet, 2007, 16(2): 223-232.
[40] Sancho RM, Law BM, Harvey K. Mutations in the LRRK2 Roc-COR tandem domain link Parkinson's disease to Wnt signalling pathways[J]. Hum Mol Genet, 2009, 18(20): 3955-3968.
[41] 孔国强,果伟. 碳酸锂的现状与进展[J]. 中国临床药学杂志, 2009,18(3): 183-185.
[42] Huang HC, Klein PS. Multiple roles for glycogen synthase kinase-3 as a drug target in Alzheimer's disease[J]. Curr Drug Targets, 2006, 7(11): 1389-1397.
[43] Caraci F, Busceti C, Biagioni F, et al. The Wnt antagonist, Dickkopf-1, as a target for the treatment of neurodegenerative disorders[J]. Neurochem Res, 2008, 33(12): 2401-2406.