Evidence map›Paper›PMID 35467252›Full record

ArticleNeurotoxicity research2022

Depletion of B7-H4 from C3H10 T1/2 Mesenchymal Stem Cells Attenuates their Immunomodulatory Therapy in Experimental Autoimmune Encephalomyelitis Mice.

Hao Li, Simao Sun, Zhou Yin, Shugang Cao, Xiaopei Ji, Xiaoyu Duan, Hanqing Gao, Mingyuan Wang, Qi Fang, Wanli Dong and 3 more

Abstract read
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In one paragraph

Article in Neurotoxicity research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 97% 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

1 citing paper in PubMed, 0 citations in OpenAlex.

  1. Article
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.

Hao Li *Department of Neurology, The First Affiliated Hospital of Soochow University, 188 Shizi Road, Suzhou, China.
Simao Sun *Department of Neurology, The First Affiliated Hospital of Soochow University, 188 Shizi Road, Suzhou, China.
Zhou Yin *Department of Neurology, The First Affiliated Hospital of Soochow University, 188 Shizi Road, Suzhou, China.
Shugang CaoDepartment of Neurology, The First Affiliated Hospital of Soochow University, 188 Shizi Road, Suzhou, China.
Xiaopei JiDepartment of Neurology, The First Affiliated Hospital of Soochow University, 188 Shizi Road, Suzhou, China.
Xiaoyu DuanDepartment of Neurology, The First Affiliated Hospital of Soochow University, 188 Shizi Road, Suzhou, China.
Hanqing GaoDepartment of Neurology, The First Affiliated Hospital of Soochow University, 188 Shizi Road, Suzhou, China.
Mingyuan WangSuzhou Red Cross Blood Center, Suzhou, 215006, China.
Qi FangDepartment of Neurology, The First Affiliated Hospital of Soochow University, 188 Shizi Road, Suzhou, China.
Wanli DongDepartment of Neurology, The First Affiliated Hospital of Soochow University, 188 Shizi Road, Suzhou, China.
Xueguang ZhangJiangsu Institute of Clinical Immunology, Jiangsu Key Laboratory of Clinical Immunology, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China.
Yanzheng GuJiangsu Institute of Clinical Immunology, Jiangsu Key Laboratory of Clinical Immunology, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China. gyz_1982@yeah.net.
Qun XueDepartment of Neurology, The First Affiliated Hospital of Soochow University, 188 Shizi Road, Suzhou, China. qxue_sz@163.com.ORCID http://orcid.org/0000-0002-7324-7982
Soochow University · CNBeijing Red Cross Blood Center · CN

Funding

Jiangsu Provincial Key Research and Development Program BE2019666the National Natural Science Foundation of China 81273269, 81601011the Natural Science Foundation of Jiangsu Province BK20211075
6 · The paper itself

Abstract

Considering the controversial issue of whether MSC therapy is effective in the treatment of multiple sclerosis, it is important to seek more powerful data to clarify the effect of MSCs. B7-H4 is a unique costimulatory molecule that belongs to the B7 ligand family and is broadly expressed in both lymphoid and non-lymphoid tissues. Previous studies have shown that B7-H4 is involved in regulating the progression of autoimmune diseases. However, its role in MSCs and stem cell transplantation remains unclear. In this study, we focus on C3H10 T1/2 cells, which are mouse-derived mesenchymal stem cells. And we investigated the role of B7-H4 in C3H10 T1/2 cells and explored its underlying mechanisms. As a result, downregulation of B7-H4 induced apoptosis and impaired the cell proliferation of C3H10 T1/2 cells. Further results showed that cells were arrested in the G0/G1 phase after knockdown of B7-H4. Furthermore, an EAE model was induced in female C57BL/6 mice by injecting MOG 35-55, and we investigated the effect of C3H10 T1/2 cell transplantation for the EAE model after downregulation of B7-H4 in vivo. We found that C3H10 cells can migrate to the area of spinal cord lesions, and depletion of B7-H4 attenuated the immunoregulatory effect of C3H10 T1/2 cells in vivo. Together, our findings suggest that B7-H4 is important for C3H10 cells to exert neurorestoration and therefore may be a potential molecular target for stem cell transplant strategies.

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalMesenchymal Stem CellsAnimalsCell ProliferationFemaleImmunomodulationMiceMice, Inbred C57BLAutoimmune diseasesB7-H4C3H10 T1/2 cellsStem cell transplantation

Identifiers

PMID35467252
OpenAlexW4224313127

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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.