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MicroRNA abundance is altered in synaptoneurosomes during prion disease.
Mol Cell Neurosci. 2016 Mar; 71:13-24.MC

Abstract

Discrepancy in synaptic structural plasticity is one of the earliest manifestations of the neurodegenerative state. In prion diseases, a reduction in synapses and dendritic spine densities is observed during preclinical disease in neurons of the cortex and hippocampus. The underlying molecular mechanisms of these alterations have not been identified but microRNAs (miRNAs), many of which are enriched at the synapse, likely regulate local protein synthesis in rapid response to stressors such as replicating prions. MiRNAs are therefore candidate regulators of these early neurodegenerative changes and may provide clues as to the molecular pathways involved. We therefore determined changes in mature miRNA abundance within synaptoneurosomes isolated from prion-infected, as compared to mock-infected animals, at asymptomatic and symptomatic stages of disease. During preclinical disease, miRNAs that are enriched in neurons including miR-124a-3p, miR-136-5p and miR-376a-3p were elevated. At later stages of disease we found increases in miRNAs that have previously been identified as deregulated in brain tissues of prion infected mice, as well as in Alzheimer's disease (AD) models. These include miR-146a-5p, miR-142-3p, miR-143-3p, miR-145a-5p, miR-451a, miR-let-7b, miR-320 and miR-150-5p. A number of miRNAs also decreased in abundance during clinical disease. These included almost all members of the related miR-200 family (miR-200a-3p, miR-200b-3p, miR-200c-3p, miR-141-3p, and miR-429-3p) and the 182 cluster (miR-182-5p and miR-183-5p).

Authors+Show Affiliations

Molecular PathoBiology, Public Health Agency of Canada, National Microbiology Laboratory, 1015 Arlington St., Winnipeg, MB R3E 3R2, Canada; Department of Medical Microbiology and Infectious Diseases, Faculty of Health Sciences, University of Manitoba, 730 William Ave., Winnipeg, MB R3E 0W3, Canada.Molecular PathoBiology, Public Health Agency of Canada, National Microbiology Laboratory, 1015 Arlington St., Winnipeg, MB R3E 3R2, Canada.Molecular PathoBiology, Public Health Agency of Canada, National Microbiology Laboratory, 1015 Arlington St., Winnipeg, MB R3E 3R2, Canada; Department of Medical Microbiology and Infectious Diseases, Faculty of Health Sciences, University of Manitoba, 730 William Ave., Winnipeg, MB R3E 0W3, Canada.Molecular PathoBiology, Public Health Agency of Canada, National Microbiology Laboratory, 1015 Arlington St., Winnipeg, MB R3E 3R2, Canada; Department of Medical Microbiology and Infectious Diseases, Faculty of Health Sciences, University of Manitoba, 730 William Ave., Winnipeg, MB R3E 0W3, Canada.Molecular PathoBiology, Public Health Agency of Canada, National Microbiology Laboratory, 1015 Arlington St., Winnipeg, MB R3E 3R2, Canada.National Centre for Foreign Animal Disease, Canadian Food Inspection Agency, 1015 Arlington St., Winnipeg, MB R3E 3M4, Canada.Viral Diseases Division, Public Health Agency of Canada, National Microbiology Laboratory, 1015 Arlington St., Winnipeg, MB R3E 3R2, Canada.Mass Spectrometry and Proteomics Core Facility, Public Health Agency of Canada, National Microbiology Laboratory, 1015 Arlington St., Winnipeg, MB R3E 3R2, Canada.Mass Spectrometry and Proteomics Core Facility, Public Health Agency of Canada, National Microbiology Laboratory, 1015 Arlington St., Winnipeg, MB R3E 3R2, Canada.Thermo Fisher Scientific, San Jose, CA, USA.Thermo Fisher Scientific, San Jose, CA, USA.Molecular PathoBiology, Public Health Agency of Canada, National Microbiology Laboratory, 1015 Arlington St., Winnipeg, MB R3E 3R2, Canada; Department of Medical Microbiology and Infectious Diseases, Faculty of Health Sciences, University of Manitoba, 730 William Ave., Winnipeg, MB R3E 0W3, Canada. Electronic address: Stephanie.Booth@phac-aspc.gc.ca.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26658803

Citation

Boese, Amrit S., et al. "MicroRNA Abundance Is Altered in Synaptoneurosomes During Prion Disease." Molecular and Cellular Neurosciences, vol. 71, 2016, pp. 13-24.
Boese AS, Saba R, Campbell K, et al. MicroRNA abundance is altered in synaptoneurosomes during prion disease. Mol Cell Neurosci. 2016;71:13-24.
Boese, A. S., Saba, R., Campbell, K., Majer, A., Medina, S., Burton, L., Booth, T. F., Chong, P., Westmacott, G., Dutta, S. M., Saba, J. A., & Booth, S. A. (2016). MicroRNA abundance is altered in synaptoneurosomes during prion disease. Molecular and Cellular Neurosciences, 71, 13-24. https://doi.org/10.1016/j.mcn.2015.12.001
Boese AS, et al. MicroRNA Abundance Is Altered in Synaptoneurosomes During Prion Disease. Mol Cell Neurosci. 2016;71:13-24. PubMed PMID: 26658803.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - MicroRNA abundance is altered in synaptoneurosomes during prion disease. AU - Boese,Amrit S, AU - Saba,Reuben, AU - Campbell,Kristyn, AU - Majer,Anna, AU - Medina,Sarah, AU - Burton,Lynn, AU - Booth,Timothy F, AU - Chong,Patrick, AU - Westmacott,Garrett, AU - Dutta,Sucharita M, AU - Saba,Julian A, AU - Booth,Stephanie A, Y1 - 2015/12/04/ PY - 2015/07/07/received PY - 2015/10/27/revised PY - 2015/12/01/accepted PY - 2015/12/15/entrez PY - 2015/12/15/pubmed PY - 2016/11/5/medline KW - Dendrite KW - MiRNA KW - Neurodegeneration KW - Prion disease KW - Synapse KW - Synaptoneurosome SP - 13 EP - 24 JF - Molecular and cellular neurosciences JO - Mol Cell Neurosci VL - 71 N2 - Discrepancy in synaptic structural plasticity is one of the earliest manifestations of the neurodegenerative state. In prion diseases, a reduction in synapses and dendritic spine densities is observed during preclinical disease in neurons of the cortex and hippocampus. The underlying molecular mechanisms of these alterations have not been identified but microRNAs (miRNAs), many of which are enriched at the synapse, likely regulate local protein synthesis in rapid response to stressors such as replicating prions. MiRNAs are therefore candidate regulators of these early neurodegenerative changes and may provide clues as to the molecular pathways involved. We therefore determined changes in mature miRNA abundance within synaptoneurosomes isolated from prion-infected, as compared to mock-infected animals, at asymptomatic and symptomatic stages of disease. During preclinical disease, miRNAs that are enriched in neurons including miR-124a-3p, miR-136-5p and miR-376a-3p were elevated. At later stages of disease we found increases in miRNAs that have previously been identified as deregulated in brain tissues of prion infected mice, as well as in Alzheimer's disease (AD) models. These include miR-146a-5p, miR-142-3p, miR-143-3p, miR-145a-5p, miR-451a, miR-let-7b, miR-320 and miR-150-5p. A number of miRNAs also decreased in abundance during clinical disease. These included almost all members of the related miR-200 family (miR-200a-3p, miR-200b-3p, miR-200c-3p, miR-141-3p, and miR-429-3p) and the 182 cluster (miR-182-5p and miR-183-5p). SN - 1095-9327 UR - https://www.unboundmedicine.com/medline/citation/26658803/MicroRNA_abundance_is_altered_in_synaptoneurosomes_during_prion_disease_ DB - PRIME DP - Unbound Medicine ER -