Cited by 182

The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

In vivo regulation of amyloid precursor protein neuronal splicing by microRNAs: APP splicing is regulated by microRNAs

Smith, Pascal, Al Hashimi, Amelle, Girard, Johanne, Delay, Charlotte, Hébert, Sébastien S.·2011·Journal of Neurochemistry

Abstract

The β-amyloid peptide that accumulate in Alzheimer's disease (AD) brain derive from proteolytic processing of the amyloid precursor protein (APP). Recent evidence suggest that microRNAs (miRNAs) participate in the post-transcriptional regulation of APP expression. Because gene dosage effects of the APP gene can cause genetic AD, dysregulation of the miRNA network could contribute significantly to disease. Here, we present evidence that, besides APP expression regulation, miRNAs are equally involved in the regulation of neuronal APP mRNA alternative splicing. Lack of miRNAs in post-mitotic neurons in vivo is associated with APP exons 7 and 8 inclusion, while ectopic expression of miR-124, an abundant neuronal-specific miRNA, reversed these effects in cultured neurons. Similar results were obtained by depletion of endogenous polypyrimidine tract binding protein 1 (PTBP1) in cells, a recognized miR-124 target gene. Furthermore, PTBP1 levels correlate with the presence of APP exons 7 and 8, while PTBP2 levels correlate with the skipping of these exons during neuronal differentiation. Finally, we show that miR-124 is down-regulated in AD brain. In sum, our results suggest that specific miRNAs are involved in the fine-tuning of APP alternative splicing in neurons. Since abnormal neuronal splicing of APP affects β-amyloid peptide production, these results could contribute to the understanding of the implication of miRNAs in brain health and disease.

Overview

Integrity signals

Registry

Crossref · 10.1111/j.1471-4159.2010.07097.x

Cites

5 of 5 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?

  • miR-124 and miR-107 are downregulated in AD brains.

    “Smith et al. [59] found that miR-124 and miR-107 were downregulated in AD brains”

    From MicroRNAs in Extracellular Vesicles of Alzheimer’s Disease (2023) · cites this paper as [59]

  • miR-9-5p, miR-16-5p, miR-29b, miR-124 and miR-206-3p were related to the generation of Aβ.

    “miR-9-5p [42,43], miR-16-5p [101], miR-29b [47], miR-124 [59] and miR-206-3p [105] were related to the generation of Aβ.”

    From MicroRNAs in Extracellular Vesicles of Alzheimer’s Disease (2023) · cites this paper as [59]

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 30

  1. Bendotti, 1988, Neuroanatomical localization and quantification of amyloid precursor protein mRNA by in situ hybridization in the brains of normal, aneuploid, and lesioned mice, Proc. Natl Acad. Sci. USA, 85, 3628, 10.1073/pnas.85.10.3628 · DOI
  2. Bergmans, 2010, Neurons generated from APP/APLP1/APLP2 triple knockout embryonic stem cells behave normally in vitro and in vivo: lack of evidence for a cell autonomous role of the amyloid precursor protein in neuronal differentiation, Stem Cells, 28, 399, 10.1002/stem.296 · DOI
  3. Bergsdorf, 2000, Identification of cis-elements regulating exon 15 splicing of the amyloid precursor protein pre-mRNA, J. Biol. Chem., 275, 2046, 10.1074/jbc.275.3.2046 · DOI
  4. Conaco, 2006, Reciprocal actions of REST and a microRNA promote neuronal identity, Proc. Natl Acad. Sci. USA, 103, 2422, 10.1073/pnas.0511041103 · DOI · Paper page
  5. De Strooper, 2010, Novel research horizons for presenilins and gamma-secretases in cell biology and disease, Annu. Rev. Cell Dev. Biol., 26, 235, 10.1146/annurev-cellbio-100109-104117 · DOI
  6. Donev, 2007, A role for SC35 and hnRNPA1 in the determination of amyloid precursor protein isoforms, Mol. Psychiatry, 12, 681, 10.1038/sj.mp.4001971 · DOI
  7. Fan, 2010, miR-20a promotes proliferation and invasion by targeting APP in human ovarian cancer cells, Acta Biochim. Biophys. Sin. (Shanghai), 42, 318, 10.1093/abbs/gmq026 · DOI
  8. Golde, 1990, Expression of beta amyloid protein precursor mRNAs: recognition of a novel alternatively spliced form and quantitation in Alzheimer’s disease using PCR, Neuron, 4, 253, 10.1016/0896-6273(90)90100-T · DOI
  9. Hebert, 2006, Regulated intramembrane proteolysis of amyloid precursor protein and regulation of expression of putative target genes, EMBO Rep., 7, 739, 10.1038/sj.embor.7400704 · DOI
  10. Hebert, 2008, Loss of microRNA cluster miR-29a/b-1 in sporadic Alzheimer’s disease correlates with increased BACE1/beta-secretase expression, Proc. Natl Acad. Sci. USA, 105, 6415, 10.1073/pnas.0710263105 · DOI · Paper page
  11. Hebert, 2010, Genetic ablation of Dicer in adult forebrain neurons results in abnormal tau hyperphosphorylation and neurodegeneration, Hum. Mol. Genet., 19, 3959, 10.1093/hmg/ddq311 · DOI
  12. Jacobsen, 1991, Quantitative measurement of alternatively spliced amyloid precursor protein mRNA expression in Alzheimer’s disease and normal brain by S1 nuclease protection analysis, Neurobiol. Aging, 12, 585, 10.1016/0197-4580(91)90090-7 · DOI
  13. Kalsotra, 2010, MicroRNAs coordinate an alternative splicing network during mouse postnatal heart development, Genes Dev., 24, 653, 10.1101/gad.1894310 · DOI · Paper page
  14. Lim, 2005, Microarray analysis shows that some microRNAs downregulate large numbers of target mRNAs, Nature, 433, 769, 10.1038/nature03315 · DOI · Paper page
  15. Liu, 2010, MicroRNA-16 targets amyloid precursor protein to potentially modulate Alzheimer’s-associated pathogenesis in SAMP8 mice, Neurobiol. Aging
  16. Lukiw, 2007, Micro-RNA speciation in fetal, adult and Alzheimer’s disease hippocampus, Neuroreport, 18, 297, 10.1097/WNR.0b013e3280148e8b · DOI · Paper page
  17. Makeyev, 2008, Multilevel regulation of gene expression by microRNAs, Science, 319, 1789, 10.1126/science.1152326 · DOI
  18. Makeyev, 2007, The MicroRNA miR-124 promotes neuronal differentiation by triggering brain-specific alternative pre-mRNA splicing, Mol. Cell, 27, 435, 10.1016/j.molcel.2007.07.015 · DOI · Paper page
  19. Menendez-Gonzalez, 2005, APP processing and the APP-KPI domain involvement in the amyloid cascade, Neurodegener. Dis., 2, 277, 10.1159/000092315 · DOI
  20. Nelson, 2010, MiR-107 is reduced in Alzheimer’s disease brain neocortex: validation study, J. Alzheimers Dis., 21, 75, 10.3233/JAD-2010-091603 · DOI · Paper page
  21. Neve, 1990, The Alzheimer amyloid precursor-related transcript lacking the beta/A4 sequence is specifically increased in Alzheimer’s disease brain, Neuron, 5, 329, 10.1016/0896-6273(90)90169-G · DOI
  22. Nunez-Iglesias, 2010, Joint genome-wide profiling of miRNA and mRNA expression in Alzheimer’s disease cortex reveals altered miRNA regulation, PLoS ONE, 5, 10.1371/journal.pone.0008898 · DOI
  23. Papagiannakopoulos, 2009, MicroRNA-124: micromanager of neurogenesis, Cell Stem Cell, 4, 375, 10.1016/j.stem.2009.04.007 · DOI
  24. Patel, 2008, MicroRNAs can regulate human APP levels, Mol. Neurodegener., 3, 10.1186/1750-1326-3-10 · DOI
  25. Poleev, 2000, A trans-acting factor, isolated by the three-hybrid system, that influences alternative splicing of the amyloid precursor protein minigene, Eur. J. Biochem., 267, 4002, 10.1046/j.1432-1327.2000.01431.x · DOI
  26. Rockenstein, 1995, Levels and alternative splicing of amyloid beta protein precursor (APP) transcripts in brains of APP transgenic mice and humans with Alzheimer’s disease, J. Biol. Chem., 270, 28257, 10.1074/jbc.270.47.28257 · DOI
  27. Shioya, 2010, Aberrant microRNA expression in the brains of neurodegenerative diseases: miR-29a decreased in Alzheimer disease brains targets neuron navigator-3, Neuropathol. Appl. Neurobiol., 36, 320, 10.1111/j.1365-2990.2010.01076.x · DOI · Paper page
  28. Tanzi, 1993, Cellular specificity and regional distribution of amyloid beta protein precursor alternative transcripts are unaltered in Alzheimer hippocampal formation, Brain Res. Mol. Brain Res., 18, 246, 10.1016/0169-328X(93)90196-V · DOI
  29. Vilardo, 2010, MicroRNA-101 regulates amyloid precursor protein expression in hippocampal neurons, J. Biol. Chem., 285, 18344, 10.1074/jbc.M110.112664 · DOI
  30. Wang, 2008, The expression of microRNA miR-107 decreases early in Alzheimer’s disease and may accelerate disease progression through regulation of beta-site amyloid precursor protein-cleaving enzyme 1, J. Neurosci., 28, 1213, 10.1523/JNEUROSCI.5065-07.2008 · DOI · Paper page

Cited by

Sorted by citations

Metadata

Authors
Smith, P., Al Hashimi, A., Girard, J., Delay, C., & Hébert, S. S.
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2010-12-02
Volume
116
Issue
2
Pages
240-247
ISSN
0022-3042
Cited by
182
References
5
Language
en

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