Evidence map›Paper›PMID 32428701›Full record

ArticleMolecular therapy. Nucleic acids2020

miRNA-98-5p Targeting IGF2BP1 Induces Mesenchymal Stem Cell Apoptosis by Modulating PI3K/Akt and p53 in Immune Thrombocytopenia.

Yanan Wang, Jiamin Zhang, Yan Su, Chencong Wang, Gaochao Zhang, Xiao Liu, Qi Chen, Meng Lv, Yingjun Chang, Jun Peng and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.6field-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

26 citing papers in PubMed, 45 citations in OpenAlex.

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  18. Immune Status and Chemokine C Receptor 7 Expression in Primary in Patients with Immune ThrombocytopeniaTurkish journal of haematology : official journal of Turkish Society of Haematology · 2022
    Article
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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

13 authors at 2 institutions in 1 country.

Yanan WangPeking University People's Hospital, Peking University Institute of Hematology, Beijing 100044, China; National Clinical Research Center for Hematologic Disease, Beijing 100044, China; Collaborative Innovation Center of Hematology, Peking University, Beijing 100044, China.
Jiamin ZhangPeking University People's Hospital, Peking University Institute of Hematology, Beijing 100044, China; National Clinical Research Center for Hematologic Disease, Beijing 100044, China; Collaborative Innovation Center of Hematology, Peking University, Beijing 100044, China.
Yan SuPeking University People's Hospital, Peking University Institute of Hematology, Beijing 100044, China; National Clinical Research Center for Hematologic Disease, Beijing 100044, China; Collaborative Innovation Center of Hematology, Peking University, Beijing 100044, China.
Chencong WangPeking University People's Hospital, Peking University Institute of Hematology, Beijing 100044, China; National Clinical Research Center for Hematologic Disease, Beijing 100044, China; Collaborative Innovation Center of Hematology, Peking University, Beijing 100044, China.
Gaochao ZhangPeking University People's Hospital, Peking University Institute of Hematology, Beijing 100044, China; National Clinical Research Center for Hematologic Disease, Beijing 100044, China; Collaborative Innovation Center of Hematology, Peking University, Beijing 100044, China.
Xiao LiuPeking University People's Hospital, Peking University Institute of Hematology, Beijing 100044, China; National Clinical Research Center for Hematologic Disease, Beijing 100044, China; Collaborative Innovation Center of Hematology, Peking University, Beijing 100044, China.
Qi ChenPeking University People's Hospital, Peking University Institute of Hematology, Beijing 100044, China; National Clinical Research Center for Hematologic Disease, Beijing 100044, China; Collaborative Innovation Center of Hematology, Peking University, Beijing 100044, China.
Meng LvPeking University People's Hospital, Peking University Institute of Hematology, Beijing 100044, China; National Clinical Research Center for Hematologic Disease, Beijing 100044, China; Collaborative Innovation Center of Hematology, Peking University, Beijing 100044, China.
Yingjun ChangPeking University People's Hospital, Peking University Institute of Hematology, Beijing 100044, China; National Clinical Research Center for Hematologic Disease, Beijing 100044, China; Collaborative Innovation Center of Hematology, Peking University, Beijing 100044, China.
Jun PengDepartment of Hematology, Qilu Hospital, Shandong University, Jinan 250012, China.
Ming HouDepartment of Hematology, Qilu Hospital, Shandong University, Jinan 250012, China.
Xiaojun HuangPeking University People's Hospital, Peking University Institute of Hematology, Beijing 100044, China; National Clinical Research Center for Hematologic Disease, Beijing 100044, China; Collaborative Innovation Center of Hematology, Peking University, Beijing 100044, China.
Xiaohui ZhangPeking University People's Hospital, Peking University Institute of Hematology, Beijing 100044, China; National Clinical Research Center for Hematologic Disease, Beijing 100044, China; Collaborative Innovation Center of Hematology, Peking University, Beijing 100044, China. Electronic address: zhangxh100@sina.com.
Peking University · CNQilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune thrombocytopenia (ITP) is a common hematological autoimmune disease, in which defective mesenchymal stem cells (MSCs) are potentially involved. Our previous study suggested that MSCs in ITP patients displayed enhanced apoptosis. MicroRNAs (miRNAs) play important roles in ITP by affecting megakaryopoiesis, platelet production and immunoregulation, whereas the roles of miRNAs in ITP-MSCs remain unknown. In a previous study, we performed microarray analysis to obtain mRNA and miRNA profiles of ITP-MSCs. In the present study, we reanalyze the data and identify miR-98-5p as a candidate miRNA contributing to MSC deficiency in ITP. miR-98-5p acts through targeting insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1), and the subsequent downregulation of insulin-like growth factor 2 (IGF-2) causes inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, which is involved in the process of MSC deficiency. Furthermore, miR-98-5p upregulates p53 by inhibiting β-transducin repeat-containing protein (β-TrCP)-dependent p53 ubiquitination. Moreover, miR-98-5p overexpression impairs the therapeutic effect of MSCs in ITP mice. All-trans retinoic acid (ATRA) protects MSCs from apoptosis by downregulating miR-98-5p, thus providing a potential therapeutic approach for ITP. Our findings demonstrate that miR-98-5p is a critical regulator of ITP-MSCs, which will help us thoroughly understand the pathogenesis of ITP.

Identifiers

PMID32428701
PMCPMC7232042
OpenAlexW3021579289

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.