全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

Noncoding RNAs in Neurodegenerative Diseases

DOI: 10.1155/2013/375852

Full-Text   Cite this paper   Add to My Lib

Abstract:

Noncoding RNAs are widely known for their various essential roles in the development of central nervous system. It involves neurogenesis, neural stem cells generation, maintenance and maturation, neurotransmission, neural network plasticity, formation of synapses, and even brain aging and DNA damage responses. In this review, we will discuss the biogenesis of microRNA, various functions of noncoding RNA's specifically microRNAs (miRNAs) that act as the chief regulators of gene expression, and focus in particular on misregulation of miRNAs which leads to several neurodegenerative diseases as well as its therapeutic outcome. Recent evidences has shown that miRNAs expression levels are changed in patients with neurodegenerative diseases; hence, miRNA can be used as a potential diagnostic biomarker and serve as an effective therapeutic tool in overcoming various neurodegenerative disease processes. 1. Introduction Genetic and environmental factors can contribute to the development of neurodegenerative diseases. Recent studies demonstrate roles for regulatory noncoding RNA molecules (ncRNAs) in normal CNS development and function and in the onset and progression of various neurodegenerative diseases. ncRNAs are functional RNA molecules expressed specifically in the central nervous system that do not encode proteins. They are classified as small ncRNAs comprising fewer than 400 nucleotides and long ncRNAs comprising more than 400 nucleotides. Small ncRNAs include ribosomal RNAs (rRNAs), transfer RNAs (tRNAs), small nucleolar RNAs (snRNAs), microRNAs (miRNAs), short small interference RNAs (siRNAs), and piwi-interacting RNAs. Long noncoding RNAs (lncRNAs) include heterogeneous regulatory molecules such as long intergenic noncoding RNAs (linc RNAs) and natural antisense transcripts (NATs) [1–3]. ncRNAs play critical roles in neuronal processes such as transcription of neuronal genes, brain morphogenesis, neuronal cell specification, and formation of memory [3]. 2. Biogenesis of MicroRNAs MicroRNAs (miRNAs) are small RNA molecules (21–23 nucleotides) involved in the regulation of gene expression that bind posttranscriptionally to the 3′-untranslated region of target mRNAs and either inhibit translation or degrade the target mRNA [4]. A single-stranded RNA, miRNA, is derived from a 70–100-nucleotide hairpin precursor called pre-miRNA that plays a key role in posttranscriptional regulation of target gene expression. Due to their small size, miRNAs are potentially a valuable tool for therapy of cancer, neurodegenerative, and cardiovascular diseases [5, 6]. The

References

[1]  I. A. Qureshi, J. S. Mattick, and M. F. Mehler, “Long non-coding RNAs in nervous system function and disease,” Brain Research, vol. 1338, pp. 20–35, 2010.
[2]  J. S. Mattick, “The central role of RNA in human development and cognition,” FEBS Letters, vol. 585, no. 11, pp. 1600–1616, 2011.
[3]  E. Salta and B. D. Strooper, “Non-coding RNAs with essential roles in neurodegenerative disorders,” The Lancet Neurology, vol. 11, no. 2, pp. 189–200, 2012.
[4]  J. Kim, K. Inoue, J. Ishii et al., “A microRNA feedback circuit in midbrain dopamine neurons,” Science, vol. 317, no. 5842, pp. 1220–1224, 2007.
[5]  M. D. Harraz, T. M. Dawson, and V. L. Dawson, “MicroRNAs in Parkinson's disease,” Journal of Chemical Neuroanatomy, vol. 42, no. 2, pp. 127–130, 2011.
[6]  N. K. Liu and X. M. Xu, “MicroRNA in central nervous system trauma and degenerative disorders,” Physiological Genomics, vol. 43, no. 10, pp. 571–580, 2011.
[7]  D. P. Bartel, “MicroRNAs: target recognition and regulatory functions,” Cell, vol. 136, no. 2, pp. 215–233, 2009.
[8]  P. T. Nelson, W. X. Wang, and B. W. Rajeev, “MicroRNAs (miRNAs) in neurodegenerative diseases,” Brain Pathology, vol. 18, no. 1, pp. 130–138, 2008.
[9]  S. Bian and T. Sun, “Functions of noncoding RNAs in neural development and neurological diseases,” Molecular Neurobiology, vol. 44, no. 3, pp. 359–373, 2011.
[10]  P. Provost, “MicroRNAs as a molecular basis for mental retardation, Alzheimer's and prion diseases,” Brain Research, vol. 1338, pp. 58–66, 2010.
[11]  L. Du and A. Pertsemlidis, “Cancer and neurodegenerative disorders: pathogenic convergence through microRNA regulation,” Journal of Molecular Cell Biology, vol. 3, no. 3, pp. 176–180, 2011.
[12]  E. Vilardo, C. Barbato, M. Ciotti, C. Cogoni, and F. Ruberti, “MicroRNA-101 regulates amyloid precursor protein expression in hippocampal neurons,” The Journal of Biological Chemistry, vol. 285, no. 24, pp. 18344–18351, 2010.
[13]  G. Wang, J. M. van der Walt, G. Mayhew et al., “Variation in the miRNA-433 binding site of FGF20 confers risk for parkinson disease by overexpression of α-synuclein,” American Journal of Human Genetics, vol. 82, no. 2, pp. 283–289, 2008.
[14]  S. S. Hebert, K. Horre, L. Nicolai et al., “Loss of microRNA cluster miR-29a/b-1 in sporadic Alzheimer's disease correlates with increased BACE1/beta-secretase expression,” Proceedings of the National Academy of the Sciences of the United States of America, vol. 105, no. 17, pp. 6415–6420, 2008.
[15]  W. X. Wang, Q. Huang, Y. Hu, A. J. Stromberg, and P. T. Nelson, “Patterns of microRNA expression in normal and early Alzheimer's disease human temporal cortex: white matter versus gray matter,” Acta Neuropathologica, vol. 121, no. 2, pp. 193–205, 2011.
[16]  V. Boissonneault, I. Plante, S. Rivest, and P. Provost, “MicroRNA-298 and microRNA-328 regulate expression of mouse β-amyloid precursor protein-converting enzyme 1,” The Journal of Biological Chemistry, vol. 284, no. 4, pp. 1971–1981, 2009.
[17]  S. Massone, I. Vassallo, G. Fiorino et al., “17A, a novel non-coding RNA, regulates GABA B alternative splicing and signaling in response to inflammatory stimuli and in Alzheimer disease,” Neurobiology of Disease, vol. 41, no. 2, pp. 308–317, 2011.
[18]  S. Massone, E. Ciarlo, S. Vella et al., “NDM29, a RNA polymerase III-dependent non-coding RNA, promotes amyloidogenic processing of APP and amyloid β secretion,” Biochimica et Biophysica Acta, vol. 1823, no. 7, pp. 1170–1177, 2012.
[19]  W. J. Lukiw, Y. Zhao, and G. C. Jian, “An NF-κB-sensitive micro RNA-146a-mediated inflammatory circuit in alzheimer disease and in stressed human brain cells,” The Journal of Biological Chemistry, vol. 283, no. 46, pp. 31315–31322, 2008.
[20]  E. Junn, K. W. Lee, S. J. Byeong, T. W. Chan, J. Y. Im, and M. M. Mouradian, “Repression of α-synuclein expression and toxicity by microRNA-7,” Proceedings of the National Academy of Sciences of the United States of America, vol. 106, no. 31, pp. 13052–13057, 2009.
[21]  E. Doxakis, “Post-transcriptional regulation of α-synuclein expression by mir-7 and mir-153,” The Journal of Biological Chemistry, vol. 285, no. 17, pp. 12726–12734, 2010.
[22]  S. Gehrke, Y. Imai, N. Sokol, and B. Lu, “Pathogenic LRRK2 negatively regulates microRNA-mediated translational repression,” Nature, vol. 466, no. 7306, pp. 637–641, 2010.
[23]  L. G. T. Morris, S. Veeriah, and T. A. Chan, “Genetic determinants at the interface of cancer and neurodegenerative disease,” Oncogene, vol. 29, no. 24, pp. 3453–3464, 2010.
[24]  Y. Zhang and R. M. Friedlander, “Using non-coding small RNAs to develop therapies for Huntington's disease,” Gene Therapy, vol. 18, no. 12, pp. 1139–1149, 2011.
[25]  R. Johnson and N. J. Buckley, “Gene dysregulation in Huntington's disease: REST, microRNAs and beyond,” Neuromolecular Medicine, vol. 11, no. 3, pp. 183–199, 2009.
[26]  S. T. Lee, K. Chu, W. S. Im et al., “Altered microRNA regulation in Huntington's disease models,” Experimental Neurology, vol. 227, no. 1, pp. 172–179, 2011.
[27]  E. Marti, L. Pantano, M. Banez-Coronel et al., “A myriad of miRNA variants in control and Huntington’s disease brain regions detected by massively parallel sequencing,” Nucleic Acids Research, vol. 38, no. 20, pp. 7219–7235, 2010.
[28]  C. Zuccato, A. Ciammola, D. Rigamonti et al., “Loss of huntingtin-mediated BDNF gene transcription in Huntington's disease,” Science, vol. 293, no. 5529, pp. 493–498, 2001.
[29]  N. Mellios, H. S. Huang, A. Grigorenko, E. Rogaev, and S. Akbarian, “A set of differentially expressed miRNAs, including miR-30a-5p, act as post-transcriptional inhibitors of BDNF in prefrontal cortex,” Human Molecular Genetics, vol. 17, no. 19, pp. 3030–3042, 2008.
[30]  R. Johnson, C. Zuccato, N. D. Belyaev, D. J. Guest, E. Cattaneo, and N. J. Buckley, “A microRNA-based gene dysregulation pathway in Huntington's disease,” Neurobiology of Disease, vol. 29, no. 3, pp. 438–445, 2008.
[31]  T. Nomura, M. Kimura, T. Horii et al., “MeCP2-dependent repression of an imprinted miR-184 released by depolarization,” Human Molecular Genetics, vol. 17, no. 8, pp. 1192–1199, 2008.
[32]  C. Conaco, S. Otto, J. J. Han, and G. Mandel, “Reciprocal actions of REST and a microRNA promote neuronal identity,” Proceedings of the National Academy of Sciences of the United States of America, vol. 103, no. 7, pp. 2422–2427, 2006.
[33]  A. N. Packer, Y. Xing, S. Q. Harper, L. Jones, and B. L. Davidson, “The bifunctional microRNA miR-9/miR-9* regulates REST and CoREST and is downregulated in Huntington's disease,” Journal of Neuroscience, vol. 28, no. 53, pp. 14341–14346, 2008.
[34]  G. S. Mack, “MicroRNA gets down to business,” Nature Biotechnology, vol. 25, no. 6, pp. 631–638, 2007.
[35]  T. A. Cooper, L. Wan, and G. Dreyfuss, “RNA and disease,” Cell, vol. 136, no. 4, pp. 777–793, 2009.
[36]  L. L. Wang, Y. Huang, G. Wang, and S. D. Chen, “The potential role of microRNA-146 in Alzheimer's disease: biomarker or therapeutic?” Medical Hypotheses, vol. 78, no. 3, pp. 398–401, 2012.
[37]  F. Modarressi, M. A. Faghihi, N. S. Patel, B. G. Sahagan, C. Wahlestedt, and M. A. Lopez-Toledano, “Knockdown of BACE1-AS Nonprotein-Coding Transcript modulates beta- amyloid related hippocampal neurogenesis,” International Journal of Alzheimer’s Disease, vol. 2011, Article ID 929042, 11 pages, 2011.
[38]  J. P. Cogswell, J. Ward, I. A. Taylor et al., “Identification of miRNA changes in Alzheimer's disease brain and CSF yields putative biomarkers and insights into disease pathways,” Journal of Alzheimer's Disease, vol. 14, no. 1, pp. 27–41, 2008.
[39]  S. Q. Harper, P. D. Staber, X. He et al., “RNA interference improves motor and neuropathological abnormalities in a Huntington's disease mouse model,” Proceedings of the National Academy of Sciences of the United States of America, vol. 102, no. 16, pp. 5820–5825, 2005.
[40]  P. Sazani and R. Kole, “Modulation of alternative splicing by antisense oligonucleotides,” Progress in Molecular and Subcellular Biology, vol. 31, pp. 217–239, 2003.
[41]  W. Feng and Y. Feng, “MicroRNAs in neural cell development and brain diseases,” Science China Life Sciences, vol. 54, no. 12, pp. 1103–1112, 2011.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133