Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 370, Issue 3, Pages 473-477Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2008.03.120
Keywords
down syndrome; microRNA; microRNA profiling; RT-PCR; in situ hybridization; cardiac; brain
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Funding
- NHLBI NIH HHS [R01 HL084498-01A2, R01 HL084498, R01 HL048848, R29 HL048848, HL084498, HL48848] Funding Source: Medline
- NIA NIH HHS [AG21912, R01 AG021912] Funding Source: Medline
- NIEHS NIH HHS [ES012241, R01 ES012241] Funding Source: Medline
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Down syndrome (DS), or Trisomy 21, is the most common genetic cause of cognitive impairment and congenital heart defects in the human population. To date, the contribution of microRNAs (miRNAs) in DS has not been investigated. Bioinformatic analyses demonstrate that human chromosome 21 (Hsa21) harbors five miRNA genes; miR-99a, let-7c, miR-125b-2, miR-155, and miR-802. MiRNA expression profiling, miRNA RT-PCR, and miRNA in situ hybridization experiments demonstrate that these miRNAs are overexpressed in fetal brain and heart specimens from individuals with DS when compared with age- and sex-matched controls. We hypothesize that trisomic 21 gene dosage overexpression of Hsa21-derived miRNAs results in the decreased expression of specific target proteins and contribute, in part, to features of the neuronal and cardiac DS phenotype. Importantly, Hsa21-derived miRNAs may provide novel therapeutic targets in the treatment of individuals with DS. (c) 2008 Elsevier Inc. All rights reserved.
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