Evidence map›Paper›PMID 31953571›Full record

ArticlePediatric cardiology2020

scaRNA1 Levels Alter Pseudouridylation in Spliceosomal RNA U2 Affecting Alternative mRNA Splicing and Embryonic Development.

Chloe K Nagasawa, Nataliya Kibiryeva, Jennifer Marshall, James E O'Brien, Douglas C Bittel

Abstract read
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In one paragraph

Article in Pediatric cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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  5. Review
  6. Epitranscriptomic Regulations in the Heart.Physiological research · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Epitranscriptomics of cardiovascular diseases (Review).International journal of molecular medicine · 2022
    Review
  14. Article
  15. Review
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

5 authors at 2 institutions in 1 country.

Chloe K NagasawaKansas City University of Medicine and Biosciences, Kansas City, MO, USA.ORCID http://orcid.org/0000-0002-4550-1381
Nataliya KibiryevaWard Family Heart Center, Children's Mercy Hospital, Kansas City, MO, USA.
Jennifer MarshallWard Family Heart Center, Children's Mercy Hospital, Kansas City, MO, USA.
James E O'BrienWard Family Heart Center, Children's Mercy Hospital, Kansas City, MO, USA.
Douglas C BittelKansas City University of Medicine and Biosciences, Kansas City, MO, USA. dbittel@kcumb.edu.
Children's Mercy Hospital · USKansas City University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The heart is the first major organ to develop during embryogenesis and must receive proper spatiotemporal signaling for proper development. Failure of proper signaling between the first and second heart fields at twenty days gestation contributes to the generation of a congenital heart defect. The most common cyanotic congenital heart defect is tetralogy of Fallot (TOF) which requires surgical intervention in the first year of life. In right ventricular tissue of infants born with TOF, the levels of scaRNA1 are reduced and mRNA splicing is dysregulated. In this study, we investigate a method of quantifying pseudouridylation levels in relation to scaRNA1 levels in spliceosomal RNA U2 in three different groups of samples: right ventricular (RV) tissue of infants born with TOF versus RV tissue from normally developing infants, scaRNA1 knockdown in primary normal cardiomyocytes derived from normally developing infants, and scaRNA1 overexpression in primary cells derived from RV tissue from infants born with TOF. We hypothesize that the amount of pseudouridylation is dependent on scaRNA1 level, compromising spliceosomal function and therefore, contributing to the generation of a congenital heart defect. Our results revealed a statistically significant decrease of pseudouridylation levels in the right ventricular tissue of infants born with TOF compared to the controls. Knocking down the scaRNA1 levels in normal primary cardiomyocytes resulted in a statistically significant decrease of pseudouridylation. Finally, an overexpression of scaRNA1 in TOF primary cells resulted in an increase in pseudouridylation levels, but it did not achieve statistical significance. Our previous research provided an association between scaRNA levels, alternative splicing, and development. Here, we demonstrate that pseudouridylation levels in spliceosomal RNA U2 is dependent on the expression level of scaRNA1. Although further investigation is needed, we believe that scaRNA expression regulates biochemical modifications to spliceosomal RNAs, adjusting the fidelity of the spliceosome, allowing for controlled alternative splicing of mRNA that is important in embryonic development. If validated, this is an underappreciated mechanism that is critical for regulating proper embryonic development.

Indexed as

RNA, Small NuclearAlternative SplicingEmbryonic DevelopmentHeartHumansInfantRNA, MessengerSpliceosomesTetralogy of FallotRNA, MessengerRNA, Small NuclearU2 small nuclear RNACongenital heart defectsEmbryonic developmentPseudouridylationSpliceosomal RNAsTetralogy of fallot

Identifiers

PMID31953571
OpenAlexW2999116636

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.