Global microRNA Expression Profiling of Caenorhabditis elegans Parkinson's Disease Models
MicroRNAs (miRNAs) play an important role in human brain development and maintenance. To search for miRNAs that may be involved in the pathogenesis of Parkinsons disease (PD), we utilized miRNA microarrays to identify potential gene expression changes in 115 annotated miRNAs in PD-associated Caenorh...
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Published in | Journal of molecular neuroscience Vol. 41; no. 1; pp. 210 - 218 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
New York
Humana Press Inc
01.05.2010
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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Summary: | MicroRNAs (miRNAs) play an important role in human brain development and maintenance. To search for miRNAs that may be involved in the pathogenesis of Parkinsons disease (PD), we utilized miRNA microarrays to identify potential gene expression changes in 115 annotated miRNAs in PD-associated
Caenorhabditis elegans
models that either overexpress human A53T α-synuclein or have mutations within the vesicular catecholamine transporter (
cat-1
) or parkin (
pdr-1
) ortholog. Here, we show that 12 specific miRNAs are differentially regulated in the animals overexpressing α-synuclein, five in
cat-1
, and three in the
pdr-1
mutants. The family of miR-64 and miR-65 are co-underexpressed in the α-synuclein transgenic and
cat-1
strains, and members of
let-7
family co-underexpressed in the α-synuclein and
pdr-1
strains;
mdl-1
and
ptc-1
genes are target candidates for miR-64 and miR-65 and are overexpressed in α-synuclein transgenic as well as miR-64/65 (tm3711) knockout animals. These results indicate that miRNAs are differentially expressed in
C. elegans
PD models and suggest a role for these molecules in disease pathogenesis. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0895-8696 1559-1166 1559-1166 |
DOI: | 10.1007/s12031-009-9325-1 |