請用此 Handle URI 來引用此文件：
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/49400完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 陳小梨 | |
| dc.contributor.author | Tung-Chien Wu | en |
| dc.contributor.author | 吳東謙 | zh_TW |
| dc.date.accessioned | 2021-06-15T11:26:57Z | - |
| dc.date.available | 2018-08-26 | |
| dc.date.copyright | 2016-08-26 | |
| dc.date.issued | 2016 | |
| dc.date.submitted | 2016-08-18 | |
| dc.identifier.citation | Aline, G., & Sotiropoulos, A. (2012). Srf: A key factor controlling skeletal muscle hypertrophy by enhancing the recruitment of muscle stem cells. Bioarchitecture, 2(3), 88-90. doi: 10.4161/bioa.20699
Alves, C. J., Dariolli, R., Jorge, F. M., Monteiro, M. R., Maximino, J. R., Martins, R. S., . . . Chadi, G. (2015). Gene expression profiling for human iPS-derived motor neurons from sporadic ALS patients reveals a strong association between mitochondrial functions and neurodegeneration. Front Cell Neurosci, 9, 289. doi: 10.3389/fncel.2015.00289 Amor, S., Puentes, F., Baker, D., & van der Valk, P. (2010). Inflammation in neurodegenerative diseases. Immunology, 129(2), 154-169. doi: 10.1111/j.1365-2567.2009.03225.x Angka, H. E., & Kablar, B. (2009). Role of skeletal muscle in the epigenetic shaping of motor neuron fate choices. Histol Histopathol, 24(12), 1579-1592. Bahler, M., & Rhoads, A. (2002). Calmodulin signaling via the IQ motif. FEBS Lett, 513(1), 107-113. Bentzinger, C. F., Wang, Y. X., & Rudnicki, M. A. (2012). Building muscle: molecular regulation of myogenesis. Cold Spring Harb Perspect Biol, 4(2). doi: 10.1101/cshperspect.a008342 Bernard-Marissal, N., Medard, J. J., Azzedine, H., & Chrast, R. (2015). Dysfunction in endoplasmic reticulum-mitochondria crosstalk underlies SIGMAR1 loss of function mediated motor neuron degeneration. Brain, 138(Pt 4), 875-890. doi: 10.1093/brain/awv008 Boido, M., & Vercelli, A. (2016). Neuromuscular Junctions as Key Contributors and Therapeutic Targets in Spinal Muscular Atrophy. Front Neuroanat, 10, 6. doi: 10.3389/fnana.2016.00006 Borisov, A. B., Dedkov, E. I., & Carlson, B. M. (2001). Interrelations of myogenic response, progressive atrophy of muscle fibers, and cell death in denervated skeletal muscle. Anat Rec, 264(2), 203-218. Braun, T., & Gautel, M. (2011). Transcriptional mechanisms regulating skeletal muscle differentiation, growth and homeostasis. Nat Rev Mol Cell Biol, 12(6), 349-361. doi: 10.1038/nrm3118 Calabria, E., Ciciliot, S., Moretti, I., Garcia, M., Picard, A., Dyar, K. A., . . . Murgia, M. (2009). NFAT isoforms control activity-dependent muscle fiber type specification. Proc Natl Acad Sci U S A, 106(32), 13335-13340. doi: 10.1073/pnas.0812911106 Chai, R. J., Vukovic, J., Dunlop, S., Grounds, M. D., & Shavlakadze, T. (2011). Striking denervation of neuromuscular junctions without lumbar motoneuron loss in geriatric mouse muscle. PLoS One, 6(12), e28090. doi: 10.1371/journal.pone.0028090 Chakkalakal, J. V., Jones, K. M., Basson, M. A., & Brack, A. S. (2012). The aged niche disrupts muscle stem cell quiescence. Nature, 490(7420), 355-360. doi: 10.1038/nature11438 Chang, S. W., Tsao, Y. P., Lin, C. Y., & Chen, S. L. (2011). NRIP, a novel calmodulin binding protein, activates calcineurin to dephosphorylate human papillomavirus E2 protein. J Virol, 85(13), 6750-6763. doi: 10.1128/JVI.02453-10 Chazin, W. J. (2011). Relating form and function of EF-hand calcium binding proteins. Acc Chem Res, 44(3), 171-179. doi: 10.1021/ar100110d Chen, H. H., Chen, W. P., Yan, W. L., Huang, Y. C., Chang, S. W., Fu, W. M., . . . Chen, S. L. (2015). NRIP is newly identified as a Z-disc protein, activating calmodulin signaling for skeletal muscle contraction and regeneration. J Cell Sci, 128(22), 4196-4209. doi: 10.1242/jcs.174441 Chen, J. C., & Goldhamer, D. J. (2003). Skeletal muscle stem cells. Reprod Biol Endocrinol, 1, 101. doi: 10.1186/1477-7827-1-101 Chen, P. H., Tsao, Y. P., Wang, C. C., & Chen, S. L. (2008). Nuclear receptor interaction protein, a coactivator of androgen receptors (AR), is regulated by AR and Sp1 to feed forward and activate its own gene expression through AR protein stability. Nucleic Acids Res, 36(1), 51-66. doi: 10.1093/nar/gkm942 Cheung, C. L., Chan, B. Y., Chan, V., Ikegawa, S., Kou, I., Ngai, H., . . . Kung, A. W. (2009). Pre-B-cell leukemia homeobox 1 (PBX1) shows functional and possible genetic association with bone mineral density variation. Hum Mol Genet, 18(4), 679-687. doi: 10.1093/hmg/ddn397 Chou, H. J., Lai, D. M., Huang, C. W., McLennan, I. S., Wang, H. D., & Wang, P. Y. (2013). BMP4 is a peripherally-derived factor for motor neurons and attenuates glutamate-induced excitotoxicity in vitro. PLoS One, 8(3), e58441. doi: 10.1371/journal.pone.0058441 Christenson, M. A., & Means, A. R. (1993). Coordinate regulation of mRNAs from multiple calmodulin genes during myoblast differentiation in vitro. J Cell Physiol, 154(2), 343-349. doi: 10.1002/jcp.1041540218 Cortes, C. J., Ling, S. C., Guo, L. T., Hung, G., Tsunemi, T., Ly, L., . . . La Spada, A. R. (2014). Muscle expression of mutant androgen receptor accounts for systemic and motor neuron disease phenotypes in spinal and bulbar muscular atrophy. Neuron, 82(2), 295-307. doi: 10.1016/j.neuron.2014.03.001 Dadon-Nachum, M., Melamed, E., & Offen, D. (2011). The 'dying-back' phenomenon of motor neurons in ALS. J Mol Neurosci, 43(3), 470-477. doi: 10.1007/s12031-010-9467-1 Dayer, A. G., Cleaver, K. M., Abouantoun, T., & Cameron, H. A. (2005). New GABAergic interneurons in the adult neocortex and striatum are generated from different precursors. J Cell Biol, 168(3), 415-427. doi: 10.1083/jcb.200407053 De Bari, C., Dell'Accio, F., Vandenabeele, F., Vermeesch, J. R., Raymackers, J. M., & Luyten, F. P. (2003). Skeletal muscle repair by adult human mesenchymal stem cells from synovial membrane. J Cell Biol, 160(6), 909-918. doi: 10.1083/jcb.200212064 de Waard, M. C., van der Pluijm, I., Zuiderveen Borgesius, N., Comley, L. H., Haasdijk, E. D., Rijksen, Y., . . . Jaarsma, D. (2010). Age-related motor neuron degeneration in DNA repair-deficient Ercc1 mice. Acta Neuropathol, 120(4), 461-475. doi: 10.1007/s00401-010-0715-9 Deacon, R. M. (2013). Measuring motor coordination in mice. J Vis Exp(75), e2609. doi: 10.3791/2609 Dedkov, E. I., Kostrominova, T. Y., Borisov, A. B., & Carlson, B. M. (2003). MyoD and myogenin protein expression in skeletal muscles of senile rats. Cell Tissue Res, 311(3), 401-416. doi: 10.1007/s00441-002-0686-9 Demonbreun, A. R., Lapidos, K. A., Heretis, K., Levin, S., Dale, R., Pytel, P., . . . McNally, E. M. (2010). Myoferlin regulation by NFAT in muscle injury, regeneration and repair. J Cell Sci, 123(Pt 14), 2413-2422. doi: 10.1242/jcs.065375 Dobrowolny, G., Giacinti, C., Pelosi, L., Nicoletti, C., Winn, N., Barberi, L., . . . Musaro, A. (2005). Muscle expression of a local Igf-1 isoform protects motor neurons in an ALS mouse model. J Cell Biol, 168(2), 193-199. doi: 10.1083/jcb.200407021 Dodge, J. C., Haidet, A. M., Yang, W., Passini, M. A., Hester, M., Clarke, J., . . . Kaspar, B. K. (2008). Delivery of AAV-IGF-1 to the CNS extends survival in ALS mice through modification of aberrant glial cell activity. Mol Ther, 16(6), 1056-1064. doi: 10.1038/mt.2008.60 Ehret, G. B., O'Connor, A. A., Weder, A., Cooper, R. S., & Chakravarti, A. (2009). Follow-up of a major linkage peak on chromosome 1 reveals suggestive QTLs associated with essential hypertension: GenNet study. Eur J Hum Genet, 17(12), 1650-1657. doi: 10.1038/ejhg.2009.94 Finley, M. F., Devata, S., & Huettner, J. E. (1999). BMP-4 inhibits neural differentiation of murine embryonic stem cells. J Neurobiol, 40(3), 271-287. Flight, Monica Hoyos. (2007). Astrocytes turn nasty. Nat Rev Drug Discov, 6(6), 434-435. Frakes, A. E., Ferraiuolo, L., Haidet-Phillips, A. M., Schmelzer, L., Braun, L., Miranda, C. J., . . . Kaspar, B. K. (2014). Microglia induce motor neuron death via the classical NF-kappaB pathway in amyotrophic lateral sclerosis. Neuron, 81(5), 1009-1023. doi: 10.1016/j.neuron.2014.01.013 Freed, Donald B. (2012). Motor speech disorders : diagnosis and treatment (2nd ed.). Clifton Park, NY: Delmar, Cengage Learning. Friese, A., Kaltschmidt, J. A., Ladle, D. R., Sigrist, M., Jessell, T. M., & Arber, S. (2009). Gamma and alpha motor neurons distinguished by expression of transcription factor Err3. Proc Natl Acad Sci U S A, 106(32), 13588-13593. doi: 10.1073/pnas.0906809106 Funakoshi, H., Belluardo, N., Arenas, E., Yamamoto, Y., Casabona, A., Persson, H., & Ibanez, C. F. (1995). Muscle-derived neurotrophin-4 as an activity-dependent trophic signal for adult motor neurons. Science, 268(5216), 1495-1499. Garcia, M. L., Fernandez, A., & Solas, M. T. (2013). Mitochondria, motor neurons and aging. J Neurol Sci, 330(1-2), 18-26. doi: 10.1016/j.jns.2013.03.019 Goldspink, G. (2012). Age-related loss of muscle mass and strength. J Aging Res, 2012, 158279. doi: 10.1155/2012/158279 Gonzalez-Freire, M., de Cabo, R., Studenski, S. A., & Ferrucci, L. (2014). The Neuromuscular Junction: Aging at the Crossroad between Nerves and Muscle. Front Aging Neurosci, 6, 208. doi: 10.3389/fnagi.2014.00208 Guo, J., Qiu, W., Soh, S. L., Wei, S., Radda, G. K., Ong, W. Y., . . . Han, W. (2013). Motor neuron degeneration in a mouse model of seipinopathy. Cell Death Dis, 4, e535. doi: 10.1038/cddis.2013.64 Hashizume, K., & Kanda, K. (1995). Differential effects of aging on motoneurons and peripheral nerves innervating the hindlimb and forelimb muscles of rats. Neurosci Res, 22(2), 189-196. Hepple, R. T. (2014). Mitochondrial involvement and impact in aging skeletal muscle. Front Aging Neurosci, 6, 211. doi: 10.3389/fnagi.2014.00211 Hikida, R. S. (2011). Aging changes in satellite cells and their functions. Curr Aging Sci, 4(3), 279-297. Hogan, P. G., Chen, L., Nardone, J., & Rao, A. (2003). Transcriptional regulation by calcium, calcineurin, and NFAT. Genes Dev, 17(18), 2205-2232. doi: 10.1101/gad.1102703 Ishibashi, J., Perry, R. L., Asakura, A., & Rudnicki, M. A. (2005). MyoD induces myogenic differentiation through cooperation of its NH2- and COOH-terminal regions. J Cell Biol, 171(3), 471-482. doi: 10.1083/jcb.200502101 Ishii, T., Miyazawa, M., Hartman, P. S., & Ishii, N. (2011). Mitochondrial superoxide anion (O(2)(-)) inducible 'mev-1' animal models for aging research. BMB Rep, 44(5), 298-305. doi: 10.5483/BMBRep.2011.44.5.298 Jackson, J. R., Kirby, T. J., Fry, C. S., Cooper, R. L., McCarthy, J. J., Peterson, C. A., & Dupont-Versteegden, E. E. (2015). Reduced voluntary running performance is associated with impaired coordination as a result of muscle satellite cell depletion in adult mice. Skelet Muscle, 5, 41. doi: 10.1186/s13395-015-0065-3 Jacob, J. M. (1998). Lumbar motor neuron size and number is affected by age in male F344 rats. Mech Ageing Dev, 106(1-2), 205-216. Kanning, K. C., Kaplan, A., & Henderson, C. E. (2010). Motor neuron diversity in development and disease. Annu Rev Neurosci, 33, 409-440. doi: 10.1146/annurev.neuro.051508.135722 Kawamura, Y., Okazaki, H., O'Brien, P. C., & Dych, P. J. (1977). Lumbar motoneurons of man: I) number and diameter histogram of alpha and gamma axons of ventral root. J Neuropathol Exp Neurol, 36(5), 853-860. Koliatsos, V. E., Cayouette, M. H., Berkemeier, L. R., Clatterbuck, R. E., Price, D. L., & Rosenthal, A. (1994). Neurotrophin 4/5 is a trophic factor for mammalian facial motor neurons. Proc Natl Acad Sci U S A, 91(8), 3304-3308. Krakora, D., Macrander, C., & Suzuki, M. (2012). Neuromuscular junction protection for the potential treatment of amyotrophic lateral sclerosis. Neurol Res Int, 2012, 379657. doi: 10.1155/2012/379657 Lamboley, C. R., Murphy, R. M., McKenna, M. J., & Lamb, G. D. (2013). Endogenous and maximal sarcoplasmic reticulum calcium content and calsequestrin expression in type I and type II human skeletal muscle fibres. J Physiol, 591(23), 6053-6068. doi: 10.1113/jphysiol.2013.265900 Lessmann, V., Gottmann, K., & Malcangio, M. (2003). Neurotrophin secretion: current facts and future prospects. Prog Neurobiol, 69(5), 341-374. Lexell, J. (1997). Evidence for nervous system degeneration with advancing age. J Nutr, 127(5 Suppl), 1011S-1013S. Li, Y., Lee, Yi, & Thompson, W. J. (2011). Changes in aging mouse neuromuscular junctions are explained by degeneration and regeneration of muscle fiber segments at the synapse. J Neurosci, 31(42), 14910-14919. doi: 10.1523/JNEUROSCI.3590-11.2011 Liu, W., Wei-LaPierre, L., Klose, A., Dirksen, R. T., & Chakkalakal, J. V. (2015). Inducible depletion of adult skeletal muscle stem cells impairs the regeneration of neuromuscular junctions. Elife, 4. doi: 10.7554/eLife.09221 Lobsiger, C. S., & Cleveland, D. W. (2007). Glial cells as intrinsic components of non-cell-autonomous neurodegenerative disease. Nat Neurosci, 10(11), 1355-1360. doi: 10.1038/nn1988 Ma, J., Smith, B. P., Smith, T. L., Walker, F. O., Rosencrance, E. V., & Koman, L. A. (2002). Juvenile and adult rat neuromuscular junctions: density, distribution, and morphology. Muscle Nerve, 26(6), 804-809. doi: 10.1002/mus.10272 Mazhar, S., & Herbst, R. (2012). The formation of complex acetylcholine receptor clusters requires MuSK kinase activity and structural information from the MuSK extracellular domain. Mol Cell Neurosci, 49(4), 475-486. doi: 10.1016/j.mcn.2011.12.007 McKinsey, T. A., Zhang, C. L., & Olson, E. N. (2000). Activation of the myocyte enhancer factor-2 transcription factor by calcium/calmodulin-dependent protein kinase-stimulated binding of 14-3-3 to histone deacetylase 5. Proc Natl Acad Sci U S A, 97(26), 14400-14405. doi: 10.1073/pnas.260501497 McManaman, J. L., Haverkamp, L. J., & Oppenheim, R. W. (1991). Skeletal muscle proteins rescue motor neurons from cell death in vivo. Adv Neurol, 56, 81-88. Meng, L., Ohman-Gault, L., Ma, L., & Krimm, R. F. (2015). Taste Bud-Derived BDNF Is Required to Maintain Normal Amounts of Innervation to Adult Taste Buds. eNeuro, 2(6). doi: 10.1523/ENEURO.0097-15.2015 Miller, K. J., Thaloor, D., Matteson, S., & Pavlath, G. K. (2000). Hepatocyte growth factor affects satellite cell activation and differentiation in regenerating skeletal muscle. Am J Physiol Cell Physiol, 278(1), C174-181. Misawa, H., Hara, M., Tanabe, S., Niikura, M., Moriwaki, Y., & Okuda, T. (2012). Osteopontin is an alpha motor neuron marker in the mouse spinal cord. J Neurosci Res, 90(4), 732-742. Muhling, T., Duda, J., Weishaupt, J. H., Ludolph, A. C., & Liss, B. (2014). Elevated mRNA-levels of distinct mitochondrial and plasma membrane Ca(2+) transporters in individual hypoglossal motor neurons of endstage SOD1 transgenic mice. Front Cell Neurosci, 8, 353. doi: 10.3389/fncel.2014.00353 Nilwik, R., Snijders, T., Leenders, M., Groen, B. B., van Kranenburg, J., Verdijk, L. B., & van Loon, L. J. (2013). The decline in skeletal muscle mass with aging is mainly attributed to a reduction in type II muscle fiber size. Exp Gerontol, 48(5), 492-498. doi: 10.1016/j.exger.2013.02.012 Olguin, H. C., Yang, Z., Tapscott, S. J., & Olwin, B. B. (2007). Reciprocal inhibition between Pax7 and muscle regulatory factors modulates myogenic cell fate determination. J Cell Biol, 177(5), 769-779. doi: 10.1083/jcb.200608122 Panaite, P. A., Kuntzer, T., Gourdon, G., Lobrinus, J. A., & Barakat-Walter, I. (2013). Functional and histopathological identification of the respiratory failure in a DMSXL transgenic mouse model of myotonic dystrophy. Dis Model Mech, 6(3), 622-631. doi: 10.1242/dmm.010512 Park, K. H. (2015). Mechanisms of Muscle Denervation in Aging: Insights from a Mouse Model of Amyotrophic Lateral Sclerosis. Aging Dis, 6(5), 380-389. doi: 10.14336/AD.2015.0506 Park, K. H., Franciosi, S., & Leavitt, B. R. (2013). Postnatal muscle modification by myogenic factors modulates neuropathology and survival in an ALS mouse model. Nat Commun, 4, 2906. doi: 10.1038/ncomms3906 Phatnani, H. P., Guarnieri, P., Friedman, B. A., Carrasco, M. A., Muratet, M., O'Keeffe, S., . . . Maniatis, T. (2013). Intricate interplay between astrocytes and motor neurons in ALS. Proc Natl Acad Sci U S A, 110(8), E756-765. doi: 10.1073/pnas.1222361110 Picard, M., Hepple, R. T., & Burelle, Y. (2012). Mitochondrial functional specialization in glycolytic and oxidative muscle fibers: tailoring the organelle for optimal function. Am J Physiol Cell Physiol, 302(4), C629-641. doi: 10.1152/ajpcell.00368.2011 Re, D. B., Le Verche, V., Yu, C., Amoroso, M. W., Politi, K. A., Phani, S., . . . Przedborski, S. (2014). Necroptosis drives motor neuron death in models of both sporadic and familial ALS. Neuron, 81(5), 1001-1008. doi: 10.1016/j.neuron.2014.01.011 Rose, U. (2004). Morphological and functional maturation of a skeletal muscle regulated by juvenile hormone. J Exp Biol, 207(Pt 3), 483-495. Ross, C. A., & Poirier, M. A. (2004). Protein aggregation and neurodegenerative disease. Nat Med, 10 Suppl, S10-17. doi: 10.1038/nm1066 Russo, S. J., & Nestler, E. J. (2013). The brain reward circuitry in mood disorders. Nat Rev Neurosci, 14(9), 609-625. doi: 10.1038/nrn3381 Rygiel, K. A., Grady, J. P., & Turnbull, D. M. (2014). Respiratory chain deficiency in aged spinal motor neurons. Neurobiol Aging, 35(10), 2230-2238. doi: 10.1016/j.neurobiolaging.2014.02.027 Sakuma, K., & Yamaguchi, A. (2011). The recent understanding of the neurotrophin's role in skeletal muscle adaptation. J Biomed Biotechnol, 2011, 201696. doi: 10.1155/2011/201696 Shepherd, Gordon M. (2004). The synaptic organization of the brain (5th ed.). Oxford ; New York: Oxford University Press. Shi, Y., Li, Z., Xu, Q., Wang, T., Li, T., Shen, J., . . . He, L. (2011). Common variants on 8p12 and 1q24.2 confer risk of schizophrenia. Nat Genet, 43(12), 1224-1227. doi: 10.1038/ng.980 Shioi, T., & Inuzuka, Y. (2012). Aging as a substrate of heart failure. J Cardiol, 60(6), 423-428. doi: 10.1016/j.jjcc.2012.07.015 Shneider, N. A., Brown, M. N., Smith, C. A., Pickel, J., & Alvarez, F. J. (2009). Gamma motor neurons express distinct genetic markers at birth and require muscle spindle-derived GDNF for postnatal survival. Neural Dev, 4, 42. doi: 10.1186/1749-8104-4-42 Song, W., Song, Y., Kincaid, B., Bossy, B., & Bossy-Wetzel, E. (2013). Mutant SOD1G93A triggers mitochondrial fragmentation in spinal cord motor neurons: neuroprotection by SIRT3 and PGC-1alpha. Neurobiol Dis, 51, 72-81. doi: 10.1016/j.nbd.2012.07.004 Stanmore, A., Bradbury, S., & Weddell, A. G. (1978). A quantitative study of peripheral nerve fibres in the mouse following the administration of drugs. 1. Age changes in untreated CBA mice from 3 to 21 months of age. J Anat, 127(Pt 1), 101-115. Stifani, N. (2014). Motor neurons and the generation of spinal motor neuron diversity. Front Cell Neurosci, 8, 293. doi: 10.3389/fncel.2014.00293 Sullivan, K. A., Kim, B., & Feldman, E. L. (2008). Insulin-like growth factors in the peripheral nervous system. Endocrinology, 149(12), 5963-5971. doi: 10.1210/en.2008-1020 Tomlinson, B. E., & Irving, D. (1977). The numbers of limb motor neurons in the human lumbosacral cord throughout life. J Neurol Sci, 34(2), 213-219. Tovar, Y. Romo L. B., Ramirez-Jarquin, U. N., Lazo-Gomez, R., & Tapia, R. (2014). Trophic factors as modulators of motor neuron physiology and survival: implications for ALS therapy. Front Cell Neurosci, 8, 61. doi: 10.3389/fncel.2014.00061 Tsai, T. C., Lee, Y. L., Hsiao, W. C., Tsao, Y. P., & Chen, S. L. (2005). NRIP, a novel nuclear receptor interaction protein, enhances the transcriptional activity of nuclear receptors. J Biol Chem, 280(20), 20000-20009. doi: 10.1074/jbc.M412169200 Valdez, G., Tapia, J. C., Kang, H., Clemenson, G. D., Jr., Gage, F. H., Lichtman, J. W., & Sanes, J. R. (2010). Attenuation of age-related changes in mouse neuromuscular synapses by caloric restriction and exercise. Proc Natl Acad Sci U S A, 107(33), 14863-14868. doi: 10.1073/pnas.1002220107 Verdijk, L. B., Snijders, T., Drost, M., Delhaas, T., Kadi, F., & van Loon, L. J. (2014). Satellite cells in human skeletal muscle; from birth to old age. Age (Dordr), 36(2), 545-547. doi: 10.1007/s11357-013-9583-2 Witzemann, V., Schwarz, H., Koenen, M., Berberich, C., Villarroel, A., Wernig, A., . . . Sakmann, B. (1996). Acetylcholine receptor epsilon-subunit deletion causes muscle weakness and atrophy in juvenile and adult mice. Proc Natl Acad Sci U S A, 93(23), 13286-13291. Wong, M., & Martin, L. J. (2010). Skeletal muscle-restricted expression of human SOD1 causes motor neuron degeneration in transgenic mice. Hum Mol Genet, 19(11), 2284-2302. doi: 10.1093/hmg/ddq106 Yablonka-Reuveni, Z., Seger, R., & Rivera, A. J. (1999). Fibroblast growth factor promotes recruitment of skeletal muscle satellite cells in young and old rats. J Histochem Cytochem, 47(1), 23-42. Yin, H., Price, F., & Rudnicki, M. A. (2013). Satellite cells and the muscle stem cell niche. Physiol Rev, 93(1), 23-67. doi: 10.1152/physrev.00043.2011 Zammit, P. S., Partridge, T. A., & Yablonka-Reuveni, Z. (2006). The skeletal muscle satellite cell: the stem cell that came in from the cold. J Histochem Cytochem, 54(11), 1177-1191. doi: 10.1369/jhc.6R6995.2006 Zammit, P. S., Relaix, F., Nagata, Y., Ruiz, A. P., Collins, C. A., Partridge, T. A., & Beauchamp, J. R. (2006). Pax7 and myogenic progression in skeletal muscle satellite cells. J Cell Sci, 119(Pt 9), 1824-1832. doi: 10.1242/jcs.02908 Zhang, Y., Ye, J., Chen, D., Zhao, X., Xiao, X., Tai, S., . . . Zhu, D. (2006). Differential expression profiling between the relative normal and dystrophic muscle tissues from the same LGMD patient. J Transl Med, 4, 53. doi: 10.1186/1479-5876-4-53 Zimprich, A., Biskup, S., Leitner, P., Lichtner, P., Farrer, M., Lincoln, S., . . . Gasser, T. (2004). Mutations in LRRK2 cause autosomal-dominant parkinsonism with pleomorphic pathology. Neuron, 44(4), 601-607. doi: 10.1016/j.neuron.2004.11.005 Zucca, F. A., Bellei, C., Giannelli, S., Terreni, M. R., Gallorini, M., Rizzio, E., . . . Zecca, L. (2006). Neuromelanin and iron in human locus coeruleus and substantia nigra during aging: consequences for neuronal vulnerability. J Neural Transm (Vienna), 113(6), 757-767. doi: 10.1007/s00702-006-0453-2 | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/49400 | - |
| dc.description.abstract | 核受體交互作用蛋白(Nuclear receptor interaction protein, NRIP)是一個鈣離子依賴性的攜鈣素(calmodulin)結合蛋白，能夠調節肌肉細胞內粒線體的活性和鈣離子的平衡以維持正常的肌肉收縮功能。在本實驗室先前的研究中，我們發現全身性NRIP基因剃除小鼠其粒線體的功能活性明顯下降，而跑動能力也有顯著受損的情形，另外，我們發現16週大的肌肉NRIP基因剃除小鼠與同週齡的正常小鼠相比，其alpha運動神經元(alpha motor neuron, α-MN)存活數量明顯減少，神經肌肉接合處(neuromuscular junction, NMJ)結構完整性變差，軸突神經支配(axonal innervation)面積縮小，我們也發現NRIP會表現在脊髓和神經肌肉接合處中，表示肌肉NRIP對於維持alpha運動神經元存活數量和神經肌肉接合處結構完整性扮演著重要的角色。然而，對於老化的小鼠而言， 肌肉NRIP是否仍有保護的作用是一件值得去探討的問題。
我們分別取下年幼(6週大)、成年(16週大)、衰老(80週大)各階段小鼠的腰段脊隨，利用免疫螢分析法去進行神經元核蛋白(neuronal nuclear protein, NeuN)和乙醯膽鹼轉化酶(choline acetyltransferase, ChAT)抗體雙染，以計數脊髓腹側角alpha運動神經元的量；利用全組織免疫螢光染色進行螢光標定的alpha-銀環蛇毒素(α-BTX)(為神經肌肉接合處形成的標記物)和神經絲蛋白(neurofilament, NF)(為運動神經元軸突標記物)抗體雙染，去分析比目魚肌中神經肌肉接合處的型態；利用免疫組織化學染色法偵測慢肌凝蛋白(slow myosin)的表現情形，以代表肌肉的組成和發育；而前肢肌肉強度和運動行為表現則是分別透過握力測試和滾輪運動測試加以分析。 實驗結果顯示在正常小數中，NRIP表現量、alpha運動神經元數量和跑動能力皆有隨著年紀增加而下降的趨勢，表示NRIP量的減少與alpha運動神經元退化和運動功能障礙息息相關，而另一方面，各週齡的肌肉NRIP基因剃除小鼠與正常小鼠相比，alpha運動神經元缺失和運動功能異常的現象更為嚴重。此外，我們發現肌肉NRIP基因剃除小鼠，隨著年紀增長其alpha運動神經元減少和運動功能衰退的趨勢與正常的小鼠相似，表示除了NRIP之外，還有其他未知的老化因子會造成運動功能上的缺陷。綜合上述的結果，我們得知肌肉NRIP基因表現的缺失會造成年紀依賴漸進性的alpha運動神經元退化和運動功能障礙。 NRIP和衛星細胞(satellite cell)皆會參與在神經肌肉接合處發育和肌肉再生過程之中，並且在老化個體中，衛星細胞數量上的減少被報導為造成老化相關運動功能障礙的成因之一。為了檢視NRIP是否會影響衛星細胞的活化或增生，我們將心臟毒素注射到正常和肌肉NRIP基因剃除小鼠的脛前肌中並分別於1天、3天及6天後，收取該肌肉檢體進行免疫螢光染色，觀察成對盒轉錄因子7(paired box transcription factor 7, Pax7)和成肌分化因子(myogenic differentiation factor, MyoD)的表現，這兩基因消長的表現模式為判斷衛星細胞處於活化或增生和定向風化的指標。從量化的實驗結果顯示，正常小鼠肌肉的衛星細胞在肌肉受損後的第一天即開始活化或增生，並隨後在第三天進行分化的動作；但肌肉NRIP基因剃除小鼠中的肌肉衛星細胞則會延至肌肉注射後的第三天才開始活化或增生，而在第六天才有明顯的定向分化發生，意味著NRIP基因表現的缺失會延遲肌肉再生的作用過程，總而言之，NRIP會影響骨骼肌再生過程中衛星細胞的活化和分化行動。 為了更加支持肌肉NRIP對於運動神經元的重要性，我們將帶有NRIP基因的腺病毒注射至肌肉NRIP基因剃除小鼠中，探討局部注入的NRIP是否能改善肌肉失養的情形。而實驗結果顯示，給予NRIP治療後9週大的肌肉NRIP基因剃除小鼠其神經肌肉接合處的大小顯著比施打GFP的對照組大，但對於alpha運動神經元數量和運動功能表現，兩組之間並無顯著的差異，表示NRIP可視為一個肌肉表現的神經營養因子(muscle-derived neurotrophic factor)有助於神經肌肉接合處的生長與形成。 | zh_TW |
| dc.description.abstract | Nuclear receptor interaction protein (NRIP) is a Ca2+-dependent calmodulin-binding protein mediating mitochondrial activity and Ca2+ homeostasis both involved in muscle contraction. In previous study, we observed that NRIP global knockout (gKO) mice have reduced mitochondrial activity and impaired running ability. Moreover, NRIP muscle-specific conditional knockout (cKO) mice have impaired alpha motor neuron (α-MN) survival, neuromuscular junction (NMJ) integrity, and axonal innervation compared to aged-matched wild-type (WT) mice at the age of 16 weeks. Also, NRIP is expressed in both the spinal cord and NMJs. It implies that NRIP in muscle may play an important role in maintaining α-MN survival and NMJ integrity. However, it is interesting to know whether the protective effect of NRIP persists in aged mice.
In our study, we isolated the lumbar spinal cord from juvenile (age 6 wk), adult (age 16 wk), and senescent mice (age 80 wk) to count the α-MN number in the ventral horn by IFA co-staining of anti-neuronal nuclear protein (NeuN) and anti-choline acetyltransferase (ChAT) antibody. The morphology of soleus (SOL) NMJs was analyzed by whole-mounting IFA co-staining fluorescently tagged alpha-bungarotoxin (α-BTX) (NMJ formation indicator) and anti-neurofilament (NF) (MN axon) antibody. The muscle development was checked by soleus IHC for slow myosin expression that represented a marker for muscle character. The forelimb muscle force and the motor behavior were examined by the grip strength assay and the rotarod test, respectively. Results showed that the NRIP level, α-MN number, grip strength, and running ability declined with age in WT mice. It implies that less NRIP expression is associated with α-MN degeneration and motor deficits. On the other hand, cKO mice exhibited significantly decreased α-MNs and performed severe motor dysfunction in comparison with WT at each age-matched littermates. Moreover, the declined trends of α-MN survival and motor functions with age were similar to WT. It indicates that in addition to NRIP, the unrevealed aging factors may play roles for the defection of motor functions. These data suggest that muscle NRIP deficiency causes age-dependent progressive α-MN degeneration and motor deficits. Both NRIP and satellite cells are involved in NMJ development and muscle regeneration. Also, loss of satellite cells in aged individuals is reported to be as one of contributing factors to cause age-related motor deficits. To examine whether NRIP affected satellite cells activation/proliferation, we injected cardiotoxin into WT and cKO mice tibialis anterior (TA) muscles and harvested at 1, 3, and 6 days after muscle injury to perform IFA staining anti-paired box transcription factor 7 (Pax7) and anti-myogenic differentiation factor (MyoD). Expression patterns of these two genes are indicators for satellite cell activation/proliferation and commitment differentiation. Quantitative data revealed that satellite cells in WT muscles began to activate/proliferate at day 1 and subsequently to differentiate at day 3 after damage; but cKO muscles delayed satellite cell activation/proliferation at day 3 and commitment differentiation at day 6 after injury. Collectively, deficiency of NRIP can delay muscle regeneration. In sum, NRIP affects satellite cells activation and differentiation during muscle regeneration in skeletal muscles. Additionally, to further support the role of NRIP in muscles and motor neuron functions, we injected cKO mice NRIP encoding by adenovirus at the age of 6 weeks to determine whether NRIP could rescue muscle dystrophy. Results showed that cKO mice treated with ad-NRIP had a larger size of NMJs than relative control (ad-GFP) at age 9 wk. However, there was no significant difference in the α-MN number and motor performance between ad-NRIP and ad-GFP treatment group. It implies that NRIP is a muscle-derived neurotrophic factor for NMJ growth. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-15T11:26:57Z (GMT). No. of bitstreams: 1 ntu-105-R03445107-1.pdf: 2154195 bytes, checksum: a918d67c205f44d2cabbf820adf97a7a (MD5) Previous issue date: 2016 | en |
| dc.description.tableofcontents | 口試委員審定書 I
致謝 II 中文摘要 III Abstract VI Chapter 1 Introduction 1 1.1 Characteristics of nuclear receptor interaction protein (NRIP) 1 1.2 The role of NRIP in muscle contraction 2 1.3 The role of NRIP in muscle regeneration 3 1.4 Motor neuron and muscle contraction 4 1.5 Autonomous and non-autonomous effects on motor neuron survival 5 1.6 Muscle-derived factors involved in motor neuron growth and maintenance 7 1.7 The role of NRIP in motor neuron 8 1.8 Aging effects on motor neuron and satellite cell 8 1.9 Aims of this study 9 Chapter 2 Materials and Methods 11 2.1 Study approval 11 2.2 Generation of muscle-specific NRIP knockout mice 11 2.3 Western blot analysis 12 2.4 Mice spinal cord isolation and frozen section preparation 13 2.5 Immunofluorescence assay of spinal motor neurons 13 2.6 Whole-mounting staining of soleus neuromuscular junction 14 2.7 Immunohistochemistry of hindlimb muscles 15 2.8 Behavior test 16 2.9 Recombinant adenovirus construction 17 2.10 Adenoviral injection 17 2.11 Statistical analysis 18 Chapter 3 Results 19 3.1 Lack of NRIP only impairs slow myofiber development in juvenile mice 19 3.2. Lack of NRIP in muscle has no effect on motor performance in juvenile mice 22 3.3 Muscle-derived NRIP maintains α-MNs survival, NMJ integrity and axonal innervation at the adult stage 24 3.4 Muscle-derived NRIP supports α-MNs survival, NMJ integrity and axonal innervation to maintain motor function at the adult stage 27 3.5 NRIP is an age-dependent in male WT mice skeletal muscle and spinal cord 28 3.6 Aging exacerbates the α-MN deficiency in senescent NRIP cKO mice 29 3.7 Aging exacerbates the motor deficits in NRIP cKO mice at the senescent age 30 3.8 Lack of muscle NRIP delays satellite cell activation in adult mice TA muscles 32 3.9 NRIP delivering by adenovirus improves NMJ growth in cKO mice 34 Chapter 4 DISCUSSION 36 Chapter 5 FIGURES 45 Chapter 6 REFERENCES 77 | |
| dc.language.iso | en | |
| dc.subject | 基因治療 | zh_TW |
| dc.subject | 衛星細胞 | zh_TW |
| dc.subject | 核受體交互作用蛋白 | zh_TW |
| dc.subject | 肌肉表現因子 | zh_TW |
| dc.subject | 運動神經元 | zh_TW |
| dc.subject | 神經肌肉接合處 | zh_TW |
| dc.subject | muscle-derived factors | en |
| dc.subject | gene therapy | en |
| dc.subject | satellite cell | en |
| dc.subject | neuromuscular junction | en |
| dc.subject | motor neuron | en |
| dc.subject | NRIP | en |
| dc.title | 肌肉NRIP表現缺失造成年齡依賴漸進性運動神經元退化和運動功能障礙作用之探討 | zh_TW |
| dc.title | Muscle-derived NRIP deficiency causes age-dependent progressive motor neuron degeneration and motor deficits | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 104-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 王培育,陳文彬,蔡力凱 | |
| dc.subject.keyword | 核受體交互作用蛋白,運動神經元,神經肌肉接合處,衛星細胞,基因治療,肌肉表現因子, | zh_TW |
| dc.subject.keyword | NRIP,motor neuron,neuromuscular junction,satellite cell,gene therapy,muscle-derived factors, | en |
| dc.relation.page | 87 | |
| dc.identifier.doi | 10.6342/NTU201603184 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2016-08-18 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 微生物學研究所 | zh_TW |
| 顯示於系所單位： | 微生物學科所 | |
文件中的檔案：
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| ntu-105-1.pdf 未授權公開取用 | 2.1 MB | Adobe PDF |
系統中的文件，除了特別指名其著作權條款之外，均受到著作權保護，並且保留所有的權利。