Evidence map›Paper›PMID 26475712›Full record

ArticleMolecular brain2015

Mesenchymal stem cells suppress neuronal apoptosis and decrease IL-10 release via the TLR2/NFκB pathway in rats with hypoxic-ischemic brain damage.

Yan Gu, Yun Zhang, Yang Bi, Jingjing Liu, Bin Tan, Min Gong, Tingyu Li, Jie Chen

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 3 pooled it
8.0field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 3 syntheses or guidelines pooled it, 63 citations in OpenAlex.

  1. Pooled it
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  5. HAX1 inhibits apoptosis and promotes maturation of neutrophils.Cell communication and signaling : CCS · 2025
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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 2 institutions in 1 country.

Yan GuChildren Nutrition Research Centre, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China. lydoctorgy@163.com.
Yun ZhangChildren Nutrition Research Centre, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China. zhangyun306@126.com.
Yang BiMinistry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China. yangbi1981@yahoo.com.
Jingjing LiuChildren Nutrition Research Centre, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China. 719954793@qq.com.
Bin TanMinistry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China. 179531172@qq.com.
Min GongChildren Nutrition Research Centre, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China. gongmeiwen1@163.com.
Tingyu LiChildren Nutrition Research Centre, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China. tyli@vip.sina.com.
Jie ChenChildren Nutrition Research Centre, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China. children_nutrition@126.com.
Children's Hospital of Chongqing Medical University · CNChongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHypoxic-ischemic brain damage (HIBD) is a major cause of infant mortality and neurological disability in children. Many studies have demonstrated that mesenchymal stem cell (MSC) transplantation facilitates the restoration of the biological function of injured tissue following HIBD via immunomodulation. This study aimed to elucidate the mechanisms by which MSCs mediate immunomodulation via the key effectors Toll-like receptor 2 (TLR2) and interleukin-10 (IL-10).

resultsWe showed that TLR2 expression in the brain of HIBD rats was upregulated following HIBD and that MSC transplantation suppressed the expression of TLR2 and the release of IL-10, thereby alleviating the learning-memory deficits of HIBD rats. Following treatment with the specific TLR2 agonist Pam3CSK4 to activate TLR2, learning-memory function became further impaired, and the levels of nuclear factor kappa B (NFκB) and Bax expression and IL-10 release were significantly increased compared with those in HIBD rats that did not receive Pam3CSK4. In vitro, we found that MSC co-culture downregulated TLR2/NFκB signaling and repressed Bax expression and IL-10 secretion in oxygen and glucose deprivation (OGD)-injured adrenal pheochromocytoma (PC12) cells. Furthermore, NFκB and Bax expression and IL-10 release were enhanced following Pam3CSK4 treatment and were decreased following siTLR2 treatment in OGD-injured PC12 cells in the presence or absence of MSCs.

conclusionsOur data indicate that TLR2 is involved in HIBD and that MSCs decrease apoptosis and improve learning-memory function in HIBD rats by suppressing the TLR2/NFκB signaling pathway via a feedback mechanism that reduces IL-10 release. These findings strongly suggest that MSC transplantation improves HIBD via the inhibition of the TLR2/NFκB pathway.

Indexed as

ApoptosisAnimalsAnimals, Newbornbcl-2-Associated X ProteinBrain IschemiaCoculture TechniquesGlucoseHypoxiaInterleukin-10LipopeptidesMemoryMesenchymal Stem CellsMesenchymal Stem Cell TransplantationNeuronsNF-kappa BOxygenbcl-2-Associated X ProteinGlucoseInterleukin-10LipopeptidesNF-kappa BOxygenPam(3)CSK(4) peptideRNA, Small InterferingToll-Like Receptor 2

Identifiers

PMID26475712
PMCPMC4609057
OpenAlexW2171800376

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.