Evidence map›Paper›PMID 27853370›Full record

ArticleInternational journal of nanomedicine

Apoptotic neuron-secreted HN12 inhibits cell apoptosis in Hirschsprung's disease.

Chunxia Du, Hua Xie, Rujin Zang, Ziyang Shen, Hongxing Li, Pingfa Chen, Xiaoqun Xu, Yankai Xia, Weibing Tang

Open access · goldAbstract read
In one paragraph

Article in International journal of nanomedicine. 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
1.2field-weighted citation impact, top 19% 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, 21 citations in OpenAlex.

  1. Review
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  12. Epigenetic Mechanisms in Hirschsprung Disease.International journal of molecular sciences · 2019
    Review
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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

9 authors at 3 institutions in 3 countries.

Chunxia DuDepartment of Pediatric Surgery, Nanjing Children's Hospital Affiliated to Nanjing Medical University; State Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health.
Hua XieDepartment of Pediatric Surgery, Nanjing Children's Hospital Affiliated to Nanjing Medical University; State Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health.
Rujin ZangDepartment of Pediatric Surgery, Nanjing Children's Hospital Affiliated to Nanjing Medical University; State Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health.
Ziyang ShenDepartment of Pediatric Surgery, Nanjing Children's Hospital Affiliated to Nanjing Medical University; State Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health.
Hongxing LiDepartment of Pediatric Surgery, Nanjing Children's Hospital Affiliated to Nanjing Medical University; State Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health.
Pingfa ChenDepartment of Pediatric Surgery, Nanjing Children's Hospital Affiliated to Nanjing Medical University; State Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health.
Xiaoqun XuDepartment of Pediatric Surgery, Nanjing Children's Hospital Affiliated to Nanjing Medical University; State Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health.
Yankai XiaState Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health; Key Laboratory of Modern Toxicology, Ministry of Education, Nanjing Medical University, Nanjing, People's Republic of China.
Weibing TangDepartment of Pediatric Surgery, Nanjing Children's Hospital Affiliated to Nanjing Medical University; State Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health.
State Key Laboratory of Reproductive MedicineNanjing Medical University · CNModern Electron (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Perturbation in apoptosis can lead to Hirschsprung's disease (HSCR), which is a genetic disorder of neural crest development. It is believed that long noncoding RNAs (lncRNAs) play a role in the progression of HSCR. This study shows that apoptotic neurons can suppress apoptosis of nonapoptotic cells by secreting exosomes that contain high levels of HN12 lncRNA. Elevated exogenous HN12 in nonapoptotic cells effectively inhibited cell apoptosis by maintaining the function of mitochondria, including the production of ATP and the release of cytochrome C. These results demonstrate that secreted lncRNAs may serve as signaling molecules mediating intercellular communication in HSCR. In addition, high HN12 levels in the circulation worked as a biomarker for predicting HSCR, providing a potential, novel, noninvasive diagnostic approach for early screening of HSCR.

Indexed as

Adenosine TriphosphateApoptosisBiomarkersCase-Control StudiesCell LineColonCytochromes cExosomesFemaleGene Expression RegulationHirschsprung DiseaseHumansInfant, NewbornIntercellular Signaling Peptides and ProteinsMaleMitochondriaAdenosine TriphosphateBiomarkersCytochromes cIntercellular Signaling Peptides and ProteinsMTRNR2L1 protein, humanProteinsRNA, Long Noncodingapoptosisexosomal long noncoding RNAHirschsprung’s diseaseintercellular communicationmitochondrianeuronal development

Identifiers

PMID27853370
PMCPMC5106231
OpenAlexW2552255080

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

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.