Evidence map›Paper›PMID 37165848›Full record

ArticleHaematologica2023

Aging-induced pseudouridine synthase 10 impairs hematopoietic stem cells.

Yuqian Wang, Zhenzhen Zhang, Hanqing He, Jinghui Song, Yang Cui, Yunan Chen, Yuan Zhuang, Xiaoting Zhang, Mo Li, Xinxiang Zhang and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Haematologica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. 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

14 authors.

Yuqian WangSchool of Pharmaceutical Sciences, Tsinghua University, Beijing 100084.
Zhenzhen ZhangSchool of Medicine, Tsinghua University, Beijing 100084.
Hanqing HeSchool of Pharmaceutical Sciences, Tsinghua University, Beijing 100084.
Jinghui SongDepartment of Bioengineering, University of California San Diego, La Jolla, CA 92093.
Yang CuiSchool of Pharmaceutical Sciences, Tsinghua University, Beijing 100084.
Yunan ChenBeijing National Laboratory for Molecular Sciences, Key Laboratory of Bioorganic Chemistry and Molecular Engineering of Ministry of Education, College of Chemistry and Molecular Engineering, Peking University, Beijing.
Yuan ZhuangDepartment of Basic Medical Sciences, School of Medicine, Institute for Immunology, Beijing Key Lab for Immunological Research on Chronic Diseases, THU-PKU Center for Life Sciences, Tsinghua University, Beijing.
Xiaoting ZhangDepartment of Basic Medical Sciences, School of Medicine, Institute for Immunology, Beijing Key Lab for Immunological Research on Chronic Diseases, THU-PKU Center for Life Sciences, Tsinghua University, Beijing.
Mo LiCenter for Reproductive Medicine, Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, 100191.
Xinxiang ZhangBeijing National Laboratory for Molecular Sciences, Key Laboratory of Bioorganic Chemistry and Molecular Engineering of Ministry of Education, College of Chemistry and Molecular Engineering, Peking University, Beijing.
Michael Q ZhangSchool of Medicine, Tsinghua University, Beijing 100084, China; MOE Key Laboratory of Bioinformatics; Bioinformatics Division and Center for Synthetic and Systems Biology, BNRist; Department of Automation, Tsinghua University, Beijing 100084, China; Department of Biological Sciences, Center for Systems Biology, the University of Texas, Richardson, TX 75080-3021. michael.zhang@utdallas.edu.
Minglei ShiSchool of Medicine, Tsinghua University, Beijing 100084. shiml79@tsinghua.edu.cn.
Chengqi YiDepartment of Basic Medical Sciences, School of Medicine, Institute for Immunology, Beijing Key Lab for Immunological Research on Chronic Diseases, THU-PKU Center for Life Sciences, Tsinghua University, Beijing. chengqi.yi@pku.edu.cn.
Jianwei WangSchool of Pharmaceutical Sciences, Tsinghua University, Beijing 100084. jianweiwang@mail.tsinghua.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aged hematopoietic stem cells (HSC) exhibit compromised reconstitution capacity and differentiation-bias towards myeloid lineage, however, the molecular mechanism behind it remains not fully understood. In this study, we observed that the expression of pseudouridine (Ψ) synthase 10 is increased in aged hematopoietic stem and progenitor cells (HSPC) and enforced protein of Ψ synthase 10 (PUS10) recapitulates the phenotype of aged HSC, which is not achieved by its Ψ synthase activity. Consistently, we observed no difference of transcribed RNA pseudouridylation profile between young and aged HSPC. No significant alteration of hematopoietic homeostasis and HSC function is observed in young Pus10-/- mice, while aged Pus10-/- mice exhibit mild alteration of hematopoietic homeostasis and HSC function. Moreover, we observed that PUS10 is ubiquitinated by E3 ubiquitin ligase CRL4DCAF1 complex and the increase of PUS10 in aged HSPC is due to aging-declined CRL4DCAF1- mediated ubiquitination degradation signaling. Taken together, this study for the first time evaluated the role of PUS10 in HSC aging and function, and provided a novel insight into HSC rejuvenation and its clinical application.

Indexed as

Intramolecular TransferasesRNAAgingAnimalsHematopoietic Stem CellsMiceIntramolecular Transferasespseudouridine synthasesRNA

Identifiers

PMID37165848
PMCPMC10542847

What Socratic 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 Socratic graph.