Evidence map›Paper›PMID 38424563›Full record

ArticleCell communication and signaling : CCS2024

Extracellular vesicles from UTX-knockout endothelial cells boost neural stem cell differentiation in spinal cord injury.

Yudong Liu, Zixiang Luo, Yong Xie, Yi Sun, Feifei Yuan, Liyuan Jiang, Hongbin Lu, Jianzhong Hu

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

4 citing papers in PubMed, 7 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

8 authors at 3 institutions in 1 country.

Yudong LiuDepartment of Spine Surgery and Orthopaedics, Xiangya Hospital, Central South University, Changsha, China.
Zixiang LuoDepartment of Spine Surgery and Orthopaedics, Xiangya Hospital, Central South University, Changsha, China.
Yong XieDepartment of Spine Surgery and Orthopaedics, Xiangya Hospital, Central South University, Changsha, China.
Yi SunDepartment of Spine Surgery and Orthopaedics, Xiangya Hospital, Central South University, Changsha, China.
Feifei YuanDepartment of Spine Surgery and Orthopaedics, Xiangya Hospital, Central South University, Changsha, China.
Liyuan JiangDepartment of Spine Surgery and Orthopaedics, Xiangya Hospital, Central South University, Changsha, China. jiangliyuanxy@csu.edu.cn.
Hongbin LuDepartment of Sports Medicine, Xiangya Hospital, Central South University, Changsha, China. hongbinlu@csu.edu.cn.
Jianzhong HuDepartment of Spine Surgery and Orthopaedics, Xiangya Hospital, Central South University, Changsha, China. jianzhonghu@csu.edu.cn.
Central South University · CNXiangya Hospital Central South University · CNSoil and Fertilizer Institute of Hunan Province · CN

Funding

National Natural Science Foundation of China 82030071Science and Technology Major Project of Changsha kh2103008
6 · The paper itself

Abstract

backgroundVascular endothelial cells are pivotal in the pathophysiological progression following spinal cord injury (SCI). The UTX (Ubiquitously Transcribed Tetratripeptide Repeat on Chromosome X) serves as a significant regulator of endothelial cell phenotype. The manipulation of endogenous neural stem cells (NSCs) offers a compelling strategy for the amelioration of SCI.

methodsTwo mouse models were used to investigate SCI: NSCs lineage-traced mice and mice with conditional UTX knockout (UTX KO) in endothelial cells. To study the effects of UTX KO on neural differentiation, we harvested extracellular vesicles (EVs) from both UTX KO spinal cord microvascular endothelial cells (SCMECs) and negative control SCMECs. These EVs were then employed to modulate the differentiation trajectory of endogenous NSCs in the SCI model.

resultsIn our NSCs lineage-traced mice model of SCI, a marked decrease in neurogenesis was observed post-injury. Notably, NSCs in UTX KO SCMECs mice showed enhanced neuronal differentiation compared to controls. RNA sequencing and western blot analyses revealed an upregulation of L1 cell adhesion molecule (L1CAM), a gene associated with neurogenesis, in UTX KO SCMECs and their secreted EVs. This aligns with the observed promotion of neurogenesis in UTX KO conditions. In vivo administration of L1CAM-rich EVs from UTX KO SCMECs (KO EVs) to the mice significantly enhanced neural differentiation. Similarly, in vitro exposure of NSCs to KO EVs resulted in increased activation of the Akt signaling pathway, further promoting neural differentiation. Conversely, inhibiting Akt phosphorylation or knocking down L1CAM negated the beneficial effects of KO EVs on NSC neuronal differentiation.

conclusionsIn conclusion, our findings substantiate that EVs derived from UTX KO SCMECs can act as facilitators of neural differentiation following SCI. This study not only elucidates a novel mechanism but also opens new horizons for therapeutic interventions in the treatment of SCI. Video Abstract.

Indexed as

Extracellular VesiclesNeural Cell Adhesion Molecule L1Neural Stem CellsSpinal Cord InjuriesAnimalsCell DifferentiationDisease Models, AnimalEndothelial CellsHistone DemethylasesMiceProto-Oncogene Proteins c-aktHistone DemethylasesNeural Cell Adhesion Molecule L1Proto-Oncogene Proteins c-aktUtx protein, mouseEpigeneticsExtracellular vesiclesNeural DifferentiationSpinal cord injuryUTX

Identifiers

PMID38424563
PMCPMC10903014
OpenAlexW4392298281

What OpenQuestion holds

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LicenceCC BY
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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.