Evidence map›Paper›PMID 30526668›Full record

ArticleStem cell research & therapy2018

MEIS2 regulates endothelial to hematopoietic transition of human embryonic stem cells by targeting TAL1.

Mengge Wang, Hongtao Wang, Yuqi Wen, Xiaoyuan Chen, Xin Liu, Jie Gao, Pei Su, Yuanfu Xu, Wen Zhou, Lihong Shi and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 49 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Mengge WangState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Tianjin, 300020, China.
Hongtao WangState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Tianjin, 300020, China.
Yuqi WenState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Tianjin, 300020, China.
Xiaoyuan ChenState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Tianjin, 300020, China.
Xin LiuState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Tianjin, 300020, China.
Jie GaoState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Tianjin, 300020, China.
Pei SuState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Tianjin, 300020, China.
Yuanfu XuState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Tianjin, 300020, China.
Wen ZhouSchool of Basic Medical Science and Cancer Research Institute, Central South University, Changsha, 410013, China.
Lihong ShiState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Tianjin, 300020, China. shilhxys@ihcams.ac.cn.
Jiaxi ZhouState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Tianjin, 300020, China. zhoujx@ihcams.ac.cn.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNInstitute of Hematology & Blood Diseases Hospital · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDespite considerable progress in the development of methods for hematopoietic differentiation, efficient generation of transplantable hematopoietic stem cells (HSCs) and other genuine functional blood cells from human embryonic stem cells (hESCs) is still unsuccessful. Therefore, a better understanding of the molecular mechanism underlying hematopoietic differentiation of hESCs is highly demanded.

methodsIn this study, by using whole-genome gene profiling, we identified Myeloid Ectopic Viral Integration Site 2 homolog (MEIS2) as a potential regulator of hESC early hematopoietic differentiation. We deleted MEIS2 gene in hESCs using the CRISPR/CAS9 technology and induced them to hematopoietic differentiation, megakaryocytic differentiation.

resultsIn this study, we found that MEIS2 deletion impairs early hematopoietic differentiation from hESCs. Furthermore, MEIS2 deletion suppresses hemogenic endothelial specification and endothelial to hematopoietic transition (EHT), leading to the impairment of hematopoietic differentiation. Mechanistically, TAL1 acts as a downstream gene mediating the function of MEIS2 during early hematopoiesis. Interestingly, unlike MEIS1, MEIS2 deletion exerts minimal effects on megakaryocytic differentiation and platelet generation from hESCs.

conclusionsOur findings advance the understanding of human hematopoietic development and may provide new insights for large-scale generation of functional blood cells for clinical applications.

Indexed as

Cell DifferentiationBase SequenceCRISPR-Cas SystemsEndothelial CellsGene DeletionHematopoiesisHematopoietic Stem CellsHomeodomain ProteinsHuman Embryonic Stem CellsHumansMegakaryocytesT-Cell Acute Lymphocytic Leukemia Protein 1Transcription FactorsHomeodomain ProteinsMEIS2 protein, humanTAL1 protein, humanT-Cell Acute Lymphocytic Leukemia Protein 1Transcription FactorsEHTHematopoiesisMEIS2

Identifiers

PMID30526668
PMCPMC6286587
OpenAlexW2903602033

What OpenQuestion holds

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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.