Evidence map›Paper›PMID 30112697›Full record

ArticleIn vitro cellular & developmental biology. Animal2018

LncRNA-uc.40 silence promotes P19 embryonic cells differentiation to cardiomyocyte via the PBX1 gene.

Rongqiang Wu, Peng Xue, Yu Wan, Shizhong Wang, Meng Gu

Abstract read
PubMed Publisher
In one paragraph

Article in In vitro cellular & developmental biology. Animal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.2field-weighted citation impact, top 49% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The molecular mechanisms of cardiac development and related diseases.Signal transduction and targeted therapy · 2024
    Review
  5. Article
  6. Review
  7. Research progress of PBX1 in developmental and regenerative medicine.International journal of medical sciences · 2023
    Review
  8. PBX1 attenuates HCell stress & chaperones · 2022
    Article
  9. 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.

Rongqiang WuMedical Research Center, The Affiliated Changzhou No.2 People's Hospital of Nanjing Medical University, Changzhou, 213003, China.
Peng XueDepartment of Pediatrics, Changzhou Children's Hospital, Nantong Medical University, Nantong City, China.
Yu WanMedical Research Center, The Affiliated Changzhou No.2 People's Hospital of Nanjing Medical University, Changzhou, 213003, China.
Shizhong WangMedical Research Center, The Affiliated Changzhou No.2 People's Hospital of Nanjing Medical University, Changzhou, 213003, China. wangshizhong_1@sina.com.
Meng GuDepartment of Pediatrics, Changzhou Children's Hospital, Nantong Medical University, Nantong City, China. 932335114@qq.com.
Nanjing Medical University · CNHangzhou Children's Hospital · CN

Funding

National Natural Science Foundation of China (CN) 814170376
6 · The paper itself

Abstract

Uc.40 is a long noncoding RNA that is highly conserved among different species, although its function is unknown. It is highly expressed in abnormal human embryonic heart. We previously reported that overexpression of uc.40 promoted apoptosis and inhibited proliferation of P19 cells, and downregulated PBX1, which was identified as a potential target gene of uc.40. The current study evaluated the effects of uc40-siRNA-44 (siRNA against uc.40) on the differentiation, proliferation, apoptosis, and mitochondrial function in P19 cells, and investigated the relationship between uc.40 and PBX1 in cardiomyocytes. The uc.40 silencing expression was confirmed by quantitative real-time polymerase chain reaction (RT-PCR). Observation of morphological changes in transfected P19 cells during different stages of differentiation revealed that uc40-siRNA-44 increased the number of cardiomyocyes. There was no significant difference in the morphology or time of differentiation between the uc40-siRNA-44 group and the control group. uc40-siRNA-44 significantly promoted proliferation of P19 cells and inhibited serum starvation-induced apoptosis. There was no significant difference in mitochondrial DNA copy number or cellular ATP level between the two groups, and ROS levels were significantly decreased in uc40-siRNA-44-transfected cells. The levels of PBX1 and myocardial markers of differentiation were examined in transfected P19 cells; uc40-siRNA-44 downregulated myocardial markers and upregulated PBX1 expression. These results suggest that uc.40 may play an important role during the differentiation of P19 cells by regulation of PBX1 to promote proliferation and inhibit apoptosis. These studies provide a foundation for further study of uc.40/PBX1 in cardiac development.

Indexed as

Cell DifferentiationGene SilencingAdenosine TriphosphateAnimalsApoptosisBiomarkersCell ProliferationDNA, MitochondrialDown-RegulationEmbryonal Carcinoma Stem CellsMatrix MetalloproteinasesMiceMitochondriaMyocardiumMyocytes, CardiacOrgan SpecificityAdenosine TriphosphateBiomarkersDNA, MitochondrialMatrix MetalloproteinasesPbx1 protein, mousePre-B-Cell Leukemia Transcription Factor 1Reactive Oxygen SpeciesRNA, Long NoncodingRNA, MessengerRNA, Small InterferingCardiomyocytesCHDP19 cellsPBX1uc40-siRNA-44

Identifiers

PMID30112697
OpenAlexW2885624678

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.