Evidence map›Paper›PMID 35301927›Full record

ArticleBioengineered2022

Mesenchymal stem cells inhibited the apoptosis of alveolar epithelial cells caused by ARDS through CXCL12/CXCR4 axis.

Xiqiang He, Chenyan Li, Hua Yin, Xiaojun Tan, Jun Yi, Shujun Tian, Yan Wang, Jian Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

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  16. Tumor Necrosis Factor-Mediators of inflammation · 2023
    Article
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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.

Xiqiang HeSurgical intensive care unit, Xiangtan Central Hospital, China.
Chenyan LiSurgical intensive care unit, Xiangtan Central Hospital, China.
Hua YinSurgical intensive care unit, Xiangtan Central Hospital, China.
Xiaojun TanSurgical intensive care unit, Xiangtan Central Hospital, China.
Jun YiSurgical intensive care unit, Xiangtan Central Hospital, China.
Shujun TianSurgical intensive care unit, Xiangtan Central Hospital, China.
Yan WangSurgical intensive care unit, Xiangtan Central Hospital, China.
Jian LiuSurgical intensive care unit, Xiangtan Central Hospital, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesenchymal stem cells (MSCs) have a wide range of anti-inflammatory and immunomodulatory effects and have been observed to have potential therapeutic potential in the clinical treatment of various diseases. We pretreated lung cancer cells A549 with tumor necrosis factor (TNF-α), knocked down the key chemokine receptor CXCR4 on MSCs using lentivirus, and induced acute respiratory distress syndrome (ARDS) mouse model using lipopolysaccharide (LPS) and CXCL12 expression in vivo by adeno-associated virus (AAV-rh10) infection in mice. By co-culturing the MSCs with A549 and in vivo experiments, we observed the effects of MSCs on cell biological functions after inflammatory stimulation, oxidative stress, and the amelioration of lung injury in ARDS mice. TNF-α inhibited A549 proliferation and promoted apoptosis, scorch death-related factor activity, and oxidative stress factor were increased and CXCL12 levels in the cell supernatant were decreased. The co-culture of MSCs was able to increase cell activity and decrease oxidative stress factor levels, and this effect was not present after the knockdown of CXCR4 in MSCs. In vivo transplantation of MSCs significantly attenuated lung injury in ARDS, inhibited serum pro-inflammatory factors in mice, and down-regulated expression of apoptotic and focal factors in lung tissues while blocking CXCR4 or CXCL12 lost the repairing effect of MSCs on ARDS lung tissues. After the co-culture of MSC and lung cancer cells, the expression of CXCR4 on the surface of lung cancer cells was significantly increased, and more CXCR4 and CXCL12 acted together to activate more pro-survival pathways and inhibit apoptosis induced by TNF-α.

Indexed as

Lung InjuryLung NeoplasmsMesenchymal Stem CellsMesenchymal Stem Cell TransplantationRespiratory Distress SyndromeAlveolar Epithelial CellsAnimalsApoptosisMiceTumor Necrosis Factor-alphaTumor Necrosis Factor-alphaacute respiratory distress syndromeapoptosisCXCL12/CXCR4 signal axisMesenchymal stem cells

Identifiers

PMID35301927
PMCPMC9161978

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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.