Evidence map›Paper›PMID 29215059›Full record

ArticleScientific reports2017

Protective effect of mesenchymal stem cells on the pressure ulcer formation by the regulation of oxidative and endoplasmic reticulum stress.

Sei-Ichiro Motegi, Akiko Sekiguchi, Akihiko Uchiyama, Akihito Uehara, Chisako Fujiwara, Sahori Yamazaki, Buddhini Perera, Hideharu Nakamura, Sachiko Ogino, Yoko Yokoyama and 3 more

Abstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing 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

31 citing papers in PubMed.

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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

13 authors.

Sei-Ichiro MotegiDepartment of Dermatology, Gunma University Graduate School of Medicine, Maebashi, Japan. smotegi@gunma-u.ac.jp.
Akiko SekiguchiDepartment of Dermatology, Gunma University Graduate School of Medicine, Maebashi, Japan.
Akihiko UchiyamaDepartment of Dermatology, Gunma University Graduate School of Medicine, Maebashi, Japan.
Akihito UeharaDepartment of Dermatology, Gunma University Graduate School of Medicine, Maebashi, Japan.
Chisako FujiwaraDepartment of Dermatology, Gunma University Graduate School of Medicine, Maebashi, Japan.
Sahori YamazakiDepartment of Dermatology, Gunma University Graduate School of Medicine, Maebashi, Japan.
Buddhini PereraDepartment of Dermatology, Gunma University Graduate School of Medicine, Maebashi, Japan.
Hideharu NakamuraDivision of Plastic Surgery, Gunma University Graduate School of Medicine, Maebashi, Japan.
Sachiko OginoDepartment of Dermatology, Gunma University Graduate School of Medicine, Maebashi, Japan.
Yoko YokoyamaDepartment of Dermatology, Gunma University Graduate School of Medicine, Maebashi, Japan.
Ryoko AkaiDivision of Cell Medicine, Department of Life Science, Medical Research Institute, Kanazawa Medical University, Ishikawa, Japan.
Takao IwawakiDivision of Cell Medicine, Department of Life Science, Medical Research Institute, Kanazawa Medical University, Ishikawa, Japan.
Osamu IshikawaDepartment of Dermatology, Gunma University Graduate School of Medicine, Maebashi, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cutaneous ischemia-reperfusion (I/R) injury is associated with the early pathogenesis of cutaneous pressure ulcers (PUs). The objective of this study was to investigate the effect of mesenchymal stem cells (MSCs) injection on the formation of PUs after I/R injury and determine the underlying mechanisms. We found that the subcutaneous injection of MSCs into areas of I/R injured skin significantly suppressed the formation of PUs. I/R-induced vascular damage, hypoxia, oxidative DNA damage, and apoptosis were decreased by MSCs injection. Oxidative stress signals detected after I/R in OKD48 (Keap1-dependent oxidative stress detector, No-48-luciferase) mice were decreased by the injection of MSCs. In cultured fibroblasts, MSCs-conditioned medium significantly inhibited oxidant-induced reactive oxygen species (ROS) generation and apoptosis. Furthermore, endoplasmic reticulum (ER) stress signals detected after I/R in ERAI (ER stress-activated indicator) mice were also decreased by the injection of MSCs. These results suggest that the injection of MSCs might protect against the development of PUs after cutaneous I/R injury by reducing vascular damage, oxidative cellular damage, oxidative stress, ER stress, and apoptosis.

Indexed as

Endoplasmic Reticulum StressMesenchymal Stem Cell TransplantationOxidative StressProtective AgentsAnimalsApoptosisMaleMesenchymal Stem CellsMiceMice, Inbred C57BLOxidation-ReductionPressure UlcerReactive Oxygen SpeciesReperfusion InjurySkin DiseasesProtective AgentsReactive Oxygen Species

Identifiers

PMID29215059
PMCPMC5719411

What OpenQuestion holds

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LicenceCC BY
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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.