Evidence map›Paper›PMID 37507770›Full record

ArticleStem cell research & therapy2023

Deacetylation of FOXP1 by HDAC7 potentiates self-renewal of mesenchymal stem cells.

Shifeng Ling, Tienan Chen, Shaojiao Wang, Wei Zhang, Rujiang Zhou, Xuechun Xia, Zhengju Yao, Ying Fan, Song Ning, Jiayin Liu and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell research & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.3field-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

7 citing papers in PubMed, 8 citations in OpenAlex.

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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

14 authors at 3 institutions in 3 countries.

Shifeng LingBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, China.
Tienan ChenBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, China.
Shaojiao WangBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, China.
Wei ZhangBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, China.
Rujiang ZhouBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, China.
Xuechun XiaBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, China.
Zhengju YaoBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, China.
Ying FanDepartment of Nephrology, Sixth People's Hospital, Shanghai Jiao Tong University, Shanghai, 200240, China.
Song NingState Key Laboratory of Reproductive Medicine, Center of Clinical Reproductive Medicine, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Jiayin LiuState Key Laboratory of Reproductive Medicine, Center of Clinical Reproductive Medicine, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Lianju QinState Key Laboratory of Reproductive Medicine, Center of Clinical Reproductive Medicine, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Haley O TuckerInstitute for Cellular and Molecular Biology, University of Texas at Austin, 1 University Station A5000, Austin, TX, 78712, USA.
Niansong WangDepartment of Nephrology, Sixth People's Hospital, Shanghai Jiao Tong University, Shanghai, 200240, China. wangniansong2012@163.com.
Xizhi GuoBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, China. xzguo2005@sjtu.edu.cn.ORCID 0000-0001-8047-6049
Shanghai Jiao Tong University · CNJiangsu Province Hospital · CNThe University of Texas at Austin · US

Funding

MAR MEDIATED GENETIC SWITCH FOR IGH ENHANCER CONTROLR01CA031534 · NCI · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI TUCKER, HALEY O · 1985 to 2012
$2.9M
NCI NIH HHS R01 CA031534
6 · The paper itself

Abstract

backgroundMesenchymal stem cells (MSCs) are widely used in a variety of tissue regeneration and clinical trials due to their multiple differentiation potency. However, it remains challenging to maintain their replicative capability during in vitro passaging while preventing their premature cellular senescence. Forkhead Box P1 (FOXP1), a FOX family transcription factor, has been revealed to regulate MSC cell fate commitment and self-renewal capacity in our previous study.

methodsMass spectra analysis was performed to identify acetylation sites in FOXP1 protein. Single and double knockout mice of FOXP1 and HDAC7 were generated and analyzed with bone marrow MSCs properties. Gene engineering in human embryonic stem cell (hESC)-derived MSCs was obtained to evaluate the impact of FOXP1 key modification on MSC self-renewal potency.

resultsFOXP1 is deacetylated and potentiated by histone deacetylase 7 (HDAC7) in MSCs. FOXP1 and HDAC7 cooperatively sustain bone marrow MSC self-renewal potency while attenuating their cellular senescence. A mutation within human FOXP1 at acetylation site (T176G) homologous to murine FOXP1 T172G profoundly augmented MSC expansion capacity during early passages.

conclusionThese findings reveal a heretofore unanticipated mechanism by which deacetylation of FOXP1 potentiates self-renewal of MSC and protects them from cellular senescence. Acetylation of FOXP1 residue T172 as a critical modification underlying MSC proliferative capacity. We suggest that in vivo gene editing of FOXP1 may provide a novel avenue for manipulating MSC capability during large-scale expansion in clinical trials.

Indexed as

Cellular SenescenceMesenchymal Stem CellsAnimalsCell DifferentiationForkhead Transcription FactorsHistone DeacetylasesHumansMiceRepressor ProteinsForkhead Transcription FactorsFOXP1 protein, humanFoxp1 protein, mouseHDAC7 protein, humanHdac7 protein, mouseHistone DeacetylasesRepressor ProteinsDeacetylationFOXP1HDAC7Mesenchymal stem cellsSelf-renewal

Identifiers

PMID37507770
PMCPMC10385979
OpenAlexW4385341762

What OpenQuestion holds

Textmetadata
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.