CoChat
Sign Up
Cited by 262

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Altered microRNA regulation in Huntington's disease models

Lee, Soon-Tae, Chu, Kon, Im, Woo-Seok, Yoon, Hye-Jin, Im, Ji-Yeon, Park, Jung-Eun, Park, Ki-Ho, Jung, Keun-Hwa, Lee, Sang Kun, Kim, Manho, Roh, Jae-Kyu·2011·Experimental Neurology
DOI 10.1016/j.expneurol.2010.10.012
Open this paper in CoChat — free account

Abstract

Huntington's disease (HD) is a genetic neurodegenerative disease caused by abnormal CAG expansion. MicroRNAs (miRNAs) are short RNA molecules regulating gene expression, and are implicated in a variety of diseases including HD. However, the profiles and regulation of miRNAs in HD are not fully understood. Here, we analyzed the miRNA expression and miRNA regulators in two transgenic models of HD, YAC128 and R6/2 mice, and in a 3-nitropropionic acid (3NP)-induced striatal degeneration rat model. After characterizing the phenotypes by behavioral tests and histological analyses, we profiled striatal miRNAs using a miRNA microarray and we measured the key molecules involved in miRNA biogenesis and function. YAC128 mice showed upregulation-dominant miRNA expressions at 5 months and downregulation-dominant expressions at 12 months. Concomitantly, the expressions of Drosha-DGCR8, Exportin-5, and Dcp1 were increased at 5months, and the expression of Dicer was decreased at 12 months. In 10-week-old R6/2 mice, downregulation was dominant in the miRNA expressions and the level of Drosha decreased concomitantly. Nine miRNAs (miR-22, miR-29c, miR-128, miR-132, miR-138, miR-218, miR-222, miR-344, and miR-674*) were commonly down-regulated in both the 12-month-old YAC128 and 10-week-old R6/2 mice. Meanwhile, 3NP rats showed dynamic changes in the miRNA profiles during disease development and a few miRNAs with altered expression. Our results show that transgenic HD mice have abnormal miRNA bi…

Overview

Integrity signals

Registry

Crossref · 10.1016/j.expneurol.2010.10.012

Cites

2 of 2 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 45

  1. Bae, 2005, p53 mediates cellular dysfunction and behavioral abnormalities in Huntington's disease, Neuron, 47, 29, 10.1016/j.neuron.2005.06.005 · DOI
  2. Beal, 1993, Neurochemical and histologic characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acid, J. Neurosci., 13, 4181, 10.1523/JNEUROSCI.13-10-04181.1993 · DOI
  3. Bizat, 2003, Calpain is a major cell death effector in selective striatal degeneration induced in vivo by 3-nitropropionate: implications for Huntington's disease, J. Neurosci., 23, 5020, 10.1523/JNEUROSCI.23-12-05020.2003 · DOI
  4. Brouillet, 2005, 3-Nitropropionic acid: a mitochondrial toxin to uncover physiopathological mechanisms underlying striatal degeneration in Huntington's disease, J. Neurochem., 95, 1521, 10.1111/j.1471-4159.2005.03515.x · DOI
  5. Cheng, 2009, miR-124 regulates adult neurogenesis in the subventricular zone stem cell niche, Nat. Neurosci., 12, 399, 10.1038/nn.2294 · DOI · Paper page
  6. Choi, 2008, Members of the miRNA-200 family regulate olfactory neurogenesis, Neuron, 57, 41, 10.1016/j.neuron.2007.11.018 · DOI
  7. Cuellar, 2008, Dicer loss in striatal neurons produces behavioral and neuroanatomical phenotypes in the absence of neurodegeneration, Proc. Natl Acad. Sci. USA, 105, 5614, 10.1073/pnas.0801689105 · DOI
  8. Ehrnhoefer, 2009, Mouse models of Huntington disease: variations on a theme, Dis. Model. Mech., 2, 123, 10.1242/dmm.002451 · DOI
  9. Gao, 2010, Reduced microRNA-218 expression is associated with high nuclear factor kappa B activation in gastric cancer, Cancer, 116, 41, 10.1002/cncr.24743 · DOI
  10. Horiguchi, 2003, Opening of mitochondrial ATP-sensitive potassium channels is a trigger of 3-nitropropionic acid-induced tolerance to transient focal cerebral ischemia in rats, Stroke, 34, 1015, 10.1161/01.STR.0000063404.27912.5B · DOI
  11. Johnson, 2008, A microRNA-based gene dysregulation pathway in Huntington's disease, Neurobiol. Dis., 29, 438, 10.1016/j.nbd.2007.11.001 · DOI · Paper page
  12. Karres, 2007, The conserved microRNA miR-8 tunes atrophin levels to prevent neurodegeneration in Drosophila, Cell, 131, 136, 10.1016/j.cell.2007.09.020 · DOI
  13. Kedersha, 2007, Mammalian stress granules and processing bodies, Methods Enzymol., 431, 61, 10.1016/S0076-6879(07)31005-7 · DOI
  14. Kim, 2009, Biogenesis of small RNAs in animals, Nat. Rev. Mol. Cell Biol., 10, 126, 10.1038/nrm2632 · DOI · Paper page
  15. Landles, 2004, Huntingtin and the molecular pathogenesis of Huntington's disease. Fourth in molecular medicine review series, EMBO Rep., 5, 958, 10.1038/sj.embor.7400250 · DOI
  16. Lee, 2003, The nuclear RNase III Drosha initiates microRNA processing, Nature, 425, 415, 10.1038/nature01957 · DOI
  17. Lee, 2004, Distinct roles for Drosophila Dicer-1 and Dicer-2 in the siRNA/miRNA silencing pathways, Cell, 117, 69, 10.1016/S0092-8674(04)00261-2 · DOI
  18. Lee, 2007, Unbiased gene expression analysis implicates the huntingtin polyglutamine tract in extra-mitochondrial energy metabolism, PLoS Genet., 3, e135, 10.1371/journal.pgen.0030135 · DOI · Paper page
  19. Lee, 2008, Atorvastatin attenuates mitochondrial toxin-induced striatal degeneration, with decreasing iNOS/c-Jun levels and activating ERK/Akt pathways, J. Neurochem., 104, 1190, 10.1111/j.1471-4159.2007.05044.x · DOI
  20. Lee, 2008, miR-19, miR-101 and miR-130 co-regulate ATXN1 levels to potentially modulate SCA1 pathogenesis, Nat. Neurosci., 11, 1137, 10.1038/nn.2183 · DOI
  21. Lee, 2009, Slowed progression in models of Huntington disease by adipose stem cell transplantation, Ann. Neurol., 66, 671, 10.1002/ana.21788 · DOI
  22. Lee, 2009, microRNAs involved in ischemic preconditioning, Stroke, 40, e114
  23. Liu, 2009, MicroRNA-138 suppresses invasion and promotes apoptosis in head and neck squamous cell carcinoma cell lines, Cancer Lett., 286, 217, 10.1016/j.canlet.2009.05.030 · DOI
  24. Lund, 2004, Nuclear export of microRNA precursors, Science, 303, 95, 10.1126/science.1090599 · DOI
  25. Maes, 2008, Murine microRNAs implicated in liver functions and aging process, Mech. Ageing Dev., 129, 534, 10.1016/j.mad.2008.05.004 · DOI
  26. Mangiarini, 1996, Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice, Cell, 87, 493, 10.1016/S0092-8674(00)81369-0 · DOI · Paper page
  27. Mittoux, 2002, Corticostriatopallidal neuroprotection by adenovirus-mediated ciliary neurotrophic factor gene transfer in a rat model of progressive striatal degeneration, J. Neurosci., 22, 4478, 10.1523/JNEUROSCI.22-11-04478.2002 · DOI
  28. Napolitano, 2008, NF-κB/NOS cross-talk induced by mitochondrial complex II inhibition: implications for Huntington's disease, Neurosci. Lett., 434, 241, 10.1016/j.neulet.2007.09.056 · DOI
  29. Pandey, 2009, miR-22 inhibits estrogen signaling by directly targeting the estrogen receptor alpha mRNA, Mol. Cell. Biol., 29, 3783, 10.1128/MCB.01875-08 · DOI
  30. Park, 2009, miR-29 miRNAs activate p53 by targeting p85 alpha and CDC42, Nat. Struct. Mol. Biol., 16, 23, 10.1038/nsmb.1533 · DOI
  31. Phillips, 2005, Abnormalities of neurogenesis in the R6/2 mouse model of Huntington's disease are attributable to the in vivo microenvironment, J. Neurosci., 25, 11564, 10.1523/JNEUROSCI.3796-05.2005 · DOI
  32. Savas, 2008, Huntington's disease protein contributes to RNA-mediated gene silencing through association with Argonaute and P bodies, Proc. Natl Acad. Sci. USA, 105, 10820, 10.1073/pnas.0800658105 · DOI
  33. Schaefer, 2007, Cerebellar neurodegeneration in the absence of microRNAs, J. Exp. Med., 204, 1553, 10.1084/jem.20070823 · DOI · Paper page
  34. Shaked, 2009, MicroRNA-132 potentiates cholinergic anti-inflammatory signaling by targeting acetylcholinesterase, Immunity, 31, 965, 10.1016/j.immuni.2009.09.019 · DOI · Paper page
  35. Slow, 2003, Selective striatal neuronal loss in a YAC128 mouse model of Huntington disease, Hum. Mol. Genet., 12, 1555, 10.1093/hmg/ddg169 · DOI
  36. St-Pierre, 2006, Suppression of reactive oxygen species and neurodegeneration by the PGC-1 transcriptional coactivators, Cell, 127, 397, 10.1016/j.cell.2006.09.024 · DOI · Paper page
  37. Sugars, 2003, Transcriptional abnormalities in Huntington disease, Trends Genet., 19, 233, 10.1016/S0168-9525(03)00074-X · DOI
  38. Terasawa, 2009, Sustained activation of ERK1/2 by NGF induces microRNA-221 and 222 in PC12 cells, FEBS J., 276, 3269, 10.1111/j.1742-4658.2009.07041.x · DOI
  39. Tsang, 2009, The miR-18a* microRNA functions as a potential tumor suppressor by targeting on K-Ras, Carcinogenesis, 30, 953, 10.1093/carcin/bgp094 · DOI
  40. Van Raamsdonk, 2005, Selective degeneration and nuclear localization of mutant huntingtin in the YAC128 mouse model of Huntington disease, Hum. Mol. Genet., 14, 3823, 10.1093/hmg/ddi407 · DOI
  41. Vandesompele, 2002, Accurate normalization of real-time quantitative RT-PCR data by geometric averaging of multiple internal control genes, Genome Biol., 3, 10.1186/gb-2002-3-7-research0034 · DOI · Paper page
  42. Xu, 2007, MicroRNA (miRNA) transcriptome of mouse retina and identification of a sensory organ-specific miRNA cluster, J. Biol. Chem., 282, 25053, 10.1074/jbc.M700501200 · DOI
  43. Zhang, 2009, MicroRNA-128 inhibits glioma cells proliferation by targeting transcription factor E2F3a, J. Mol. Med., 87, 43, 10.1007/s00109-008-0403-6 · DOI · Paper page
  44. Zuccato, 2003, Huntingtin interacts with REST/NRSF to modulate the transcription of NRSE-controlled neuronal genes, Nat. Genet., 35, 76, 10.1038/ng1219 · DOI · Paper page
  45. Zuccato, 2007, Widespread disruption of repressor element-1 silencing transcription factor/neuron-restrictive silencer factor occupancy at its target genes in Huntington's disease, J. Neurosci., 27, 6972, 10.1523/JNEUROSCI.4278-06.2007 · DOI · Paper page

Cited by

Sorted by citations

Metadata

Authors
Lee, S.-T., Chu, K., Im, W.-S., Yoon, H.-J., Im, J.-Y., Park, J.-E., Park, K.-H., Jung, K.-H., Lee, S. K., Kim, M., & Roh, J.-K.
Venue
Experimental Neurology
Publisher
Elsevier BV
Published
2011-01
Volume
227
Issue
1
Pages
172-179
ISSN
0014-4886
DOI
10.1016/j.expneurol.2010.10.012
Cited by
262
References
2
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Funders
  • Research Center for Rare Diseases (A080588)
  • Korea Health 21 R&D Project (A092058, FPR08K1301-02210)
  • WCU Neurocytomics
  • Seoul National University Hospital (03-2009-002)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review