Evidence map›Paper›PMID 39181924›Full record

ArticleScientific reports2024

Mesenchymal stem cells from adipose tissue prone to lose their stemness associated markers in obesity related stress conditions.

Sura Hilal Ahmed Al-Sammarraie, Şerife Ayaz-Güner, Mustafa Burak Acar, Ahmet Şimşek, Betül Seyhan Sınıksaran, Habibe Damla Bozalan, Miray Özkan, Recep Saraymen, Munis Dündar, Servet Özcan

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Review
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  8. Adipose-Derived Extracellular Vesicles and Intercellular Crosstalk With Skeletal Muscle: Implications for Sarcopenic Obesity and Metabolic Dysregulation.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
    Review
  9. Prenatal Exposure to PMEnvironment & health (Washington, D.C.) · 2025
    Article
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  11. 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

10 authors.

Sura Hilal Ahmed Al-SammarraieGenome and Stem Cell Center, GENKÖK, Erciyes University, Kayseri, Turkey.
Şerife Ayaz-GünerDepartment of Molecular Biology and Genetics, Izmir Institute of Technology, Izmir, Turkey.
Mustafa Burak AcarGenome and Stem Cell Center, GENKÖK, Erciyes University, Kayseri, Turkey.
Ahmet ŞimşekGenome and Stem Cell Center, GENKÖK, Erciyes University, Kayseri, Turkey.
Betül Seyhan SınıksaranDepartment of Medical Genetics, Faculty of Medicine, Erciyes University, Kayseri, Turkey.
Habibe Damla BozalanGenome and Stem Cell Center, GENKÖK, Erciyes University, Kayseri, Turkey.
Miray ÖzkanGenome and Stem Cell Center, GENKÖK, Erciyes University, Kayseri, Turkey.
Recep SaraymenDepartment of Biochemistry, Private Tekden Hospital, Kayseri, Turkey.
Munis DündarDepartment of Medical Genetics, Faculty of Medicine, Erciyes University, Kayseri, Turkey.
Servet ÖzcanGenome and Stem Cell Center, GENKÖK, Erciyes University, Kayseri, Turkey. ozcan@erciyes.edu.tr.

Funding

Erciyes University Research Project Fund FYL-2019-9731
6 · The paper itself

Abstract

Obesity is a health problem characterized by large expansion of adipose tissue. During this expansion, genotoxic stressors can be accumulated and negatively affect the mesenchymal stem cells (MSCs) of adipose tissue. Due to the oxidative stress generated by these genotoxic stressors, senescence phenotype might be observed in adipose tissue MSCs. Senescent MSCs lose their proliferations and differentiation properties and secrete senescence-associated molecules to their niche thus triggering senescence for the rest of the tissue. Accumulation of senescent cells in adipose tissue results in decreased tissue regeneration and functional impairment not only in the close vicinity but also in the other tissues. Here we hypothesized that declined tissue regeneration might be associated with loss of stemness markers in MSCs population. We analyzed the expression of several stemness-associated genes of in vitro cultured MSCs originated from adipose tissue of high-fat diet and normal diet mice models. Since the heterogenous MSCs population covers a small percentage of the pluripotent stem cells, which have roles in proliferation and tissue regeneration, we measured the percentage of these cells via TRA-1-60 pluripotent state antigen. Additionally, by conducting a shotgun proteomic approach using LC-MS/MS, whole cell proteome of the adipose tissue MSCs of high-fat diet and normal diet mice were analyzed and identified proteins were evaluated via gene ontology and PPI network analysis. MSCs of obese mice showed senescent phenotype and altered cell cycle distribution due to a hostile environment with oxidative stress in adipose tissue where they reside. Additionally, the number of pluripotent markers expressing cells declined in the MSC population of the high-fat diet mice. Gene expression analysis evidenced the loss of stemness with a decrease in the expression of stemness-associated genes. Of the proteomic comparison of the normal and the high-fat diet group, MSCs revealed that stemness-associated molecules were decreased while inflammation and senescence-associated phenotypes emerged in obese mice MSCs. Our results showed us that the MSCs of adipose tissue may lose their stemness properties due to obesity-associated stress conditions.

Indexed as

Adipose TissueBiomarkersCellular SenescenceDiet, High-FatMesenchymal Stem CellsObesityAnimalsCell DifferentiationCell ProliferationCells, CulturedMaleMiceMice, Inbred C57BLOxidative StressProteomicsBiomarkersObesitySenescenceStemness

Identifiers

PMID39181924
PMCPMC11344827

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LicenceCC BY-NC-ND
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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.