Evidence map›Paper›PMID 25869329›Full record

ArticleBiochimica et biophysica acta2015

Chromosome 21-derived hsa-miR-155-5p regulates mitochondrial biogenesis by targeting Mitochondrial Transcription Factor A (TFAM).

Adolfo Quiñones-Lombraña, Javier G Blanco

Abstract read
In one paragraph

Article in Biochimica et biophysica acta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  7. Article
  8. The Role of MicroRNAs in Mitochondria-Mediated Eye Diseases.Frontiers in cell and developmental biology · 2021
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Mouse models of Down syndrome: gene content and consequences.Mammalian genome : official journal of the International Mammalian Genome Society · 2016
    Review
  16. Review
  17. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Adolfo Quiñones-LombrañaDepartment of Pharmaceutical Sciences, University at Buffalo, The State University of New York, USA.
Javier G BlancoDepartment of Pharmaceutical Sciences, University at Buffalo, The State University of New York, USA. Electronic address: jgblanco@buffalo.edu.
University at Buffalo, State University of New York · US

Funding

PHARMACOGENETICS OF HUMAN CARBONYL REDUCTASESR01GM073646 · NIGMS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI BLANCO, JAVIER GUILLERMO · 2005 to 2019
$4.1M
Characterization of Cardiac Mitochondrial DNA in Donors with Down SyndromeR03HD076055 · NICHD · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI BLANCO, JAVIER GUILLERMO · 2014 to 2015
$157k
NICHD NIH HHS R03 HD076055NICHD NIH HHS R03HD076055NIGMS NIH HHS R01 GM073646NIGMS NIH HHS R01GM073646
6 · The paper itself

Abstract

The regulation of mitochondrial biogenesis is under the control of nuclear genes including the master Mitochondrial Transcription Factor A (TFAM). Recent evidence suggests that the expression of TFAM is regulated by microRNAs (miRNAs) in various cellular contexts. Here, we show that hsa-miR-155-5p, a prominent miRNA encoded in chromosome 21, controls the expression of TFAM at the post-transcriptional level. In human fibroblasts derived from a diploid donor, downregulation of TFAM by hsa-miR-155-5p decreased mitochondrial DNA (mtDNA) content. In contrast, downregulation of TFAM by hsa-miR-155-5p did not decrease mtDNA content in fibroblasts derived from a donor with Down syndrome (DS, trisomy 21). In line, downregulation of mitochondrial TFAM levels through hsa-miR-155-5p decreased mitochondrial mass in diploid fibroblasts but not in trisomic cells. Due to the prevalence of mitochondrial dysfunction and cardiac abnormalities in subjects with DS, we examined the presence of potential associations between hsa-miR-155-5p and TFAM expression in heart samples from donors with and without DS. There were significant negative associations between hsa-miR-155-5p and TFAM expression in heart samples from donors with and without DS. These results suggest that regulation of TFAM by hsa-miR-155-5p impacts mitochondrial biogenesis in the diploid setting but not in the DS setting.

Indexed as

Mitochondrial TurnoverAnimalsCase-Control StudiesCells, CulturedCHO CellsChromosomes, Human, Pair 21CricetinaeCricetulusDNA-Binding ProteinsDNA, MitochondrialDown SyndromeFibroblastsHumansMicroRNAsMitochondrial ProteinsMyocytes, CardiacDNA-Binding ProteinsDNA, MitochondrialMicroRNAsMIRN155 microRNA, humanMitochondrial ProteinsTFAM protein, humanTranscription FactorsDown syndromeHsa-miR-155-5pMitochondrial biogenesisTFAM

Identifiers

PMID25869329
PMCPMC4433801
OpenAlexW2000429523

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.