Evidence map›Paper›PMID 30778047›Full record

ArticleCell death & disease2019

H19 potentiates let-7 family expression through reducing PTBP1 binding to their precursors in cholestasis.

Li Zhang, Zhihong Yang, Wendong Huang, Jianguo Wu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. PTBP1 as a potential regulator of disease.Molecular and cellular biochemistry · 2024
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Crosstalk between long noncoding RNA and microRNA in Cancer.Cellular oncology (Dordrecht, Netherlands) · 2023
    Review
  17. Review
  18. Article
  19. Article
  20. 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

4 authors at 4 institutions in 1 country.

Li ZhangDepartment of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
Zhihong YangDivision of Gastroenterology and Hepatology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Wendong HuangDepartment of Diabetes Complications and Metabolism, Diabetes and Metabolism Research Institute, Beckman Research Institute, City of Hope National Medical Center, Duarte, CA, 91010, USA.
Jianguo WuVeterans Affairs Connecticut Healthcare System, West Haven, CT, 06516, USA. jianguo.wu@uconn.edu.ORCID http://orcid.org/0000-0001-9801-5267
City Of Hope National Medical Center · USIndiana University School of MedicineThe University of Texas MD Anderson Cancer Center · USUniversity of Connecticut · US

Funding

MiRNAs in hepatocellular carcinoma development and treatmentR01CA139158 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI HUANG, WENDONG, YU, HUA E · 2011 to 2021
$3.7M
Integrating LncRNA to Methionine Metabolism in Alcoholic Fatty LiverK01AA026385 · NIAAA · INDIANA UNIVERSITY INDIANAPOLIS · PI YANG, ZHIHONG · 2018 to 2022
$807k
Circadian Clock Regulation of Alcoholic Liver DiseaseI01BX002634 · VA · VA CONNECTICUT HEALTHCARE SYSTEM · PI WANG, LI · 2016 to 2019
–
BLRD VA I01 BX002634NCI NIH HHS R01 CA139158NIAAA NIH HHS K01 AA026385
6 · The paper itself

Abstract

Cholestasis induces the hepatic long non-coding RNA H19, which promotes the progression of cholestatic liver fibrosis. However, microRNAs that are dysregulated by H19 during cholestasis remain elusive. Using miRNA-sequencing analysis followed by qPCR validation, we identified marked upregulation of eight members of the let-7 family in cholestatic livers by bile duct ligation (BDL) and H19 overexpression. In particular, the expression of let-7a-1/7d/7f-1 was highly induced in H19-BDL livers but decreased in H19KO-BDL livers. Interestingly, H19 decreased the nuclear let-7 precursors as well as the primary transcripts of let-7a-1/7d/7f-1 levels in BDL mouse livers. Bioinformatics, RNA pull-down, and RNA immunoprecipitation (RIP) assays revealed that the crucial RNA-binding protein polypyrimidine tract-binding protein 1 (PTBP1), an H19 interaction partner, interacted with the precursors of let-7a-1 and let-7d and suppressed their maturation. Both PTBP1 and let-7 expression was differentially regulated by different bile acid species in hepatocyte and cholangiocyte cells. Further, H19 negatively regulated PTBP1's mRNA and protein levels but did not affect its subcellular distribution in BDL mouse livers. Moreover, we found that H19 restrained but PTBP1 facilitated the bioavailability of let-7 miRNAs to their targets. Taken together, this study revealed for the first time that H19 promoted let-7 expression by decreasing PTBP1's expression level and its binding to the let-7 precursors in cholestasis.

Indexed as

AnimalsBile Acids and SaltsBile DuctsDisease Models, AnimalHepatocytesHeterogeneous-Nuclear RibonucleoproteinsLiverLiver Cirrhosis, BiliaryMaleMiceMice, Inbred C57BLMice, KnockoutMicroRNAsPolypyrimidine Tract-Binding ProteinRNA, Long NoncodingBile Acids and SaltsH19 long non-coding RNAHeterogeneous-Nuclear RibonucleoproteinsMicroRNAsmirnlet7 microRNA, mousePolypyrimidine Tract-Binding ProteinPtbp1 protein, mouseRNA, Long Noncoding

Identifiers

PMID30778047
PMCPMC6379488
OpenAlexW2913790812

What OpenQuestion holds

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LicenceCC BY
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.