Mesenchymal stem cells from adipose tissue prone to lose their stemness associated markers in obesity related stress conditions
- Sura Hilal Ahmed Al-Sammarraie 1,2, Şerife Ayaz-Güner 3, Mustafa Burak Acar 1,2,4, Ahmet Şimşek 1, Betül Seyhan Sınıksaran 5, Habibe Damla Bozalan 1, Miray Özkan 1, Recep Saraymen 6, Munis Dündar 5, Servet Özcan 7,8
- 1Genome and Stem Cell Center, GENKÖK, Erciyes University, Kayseri, Turkey.
- 2Department of Experimental Medicine, Luigi Vanvitelli Campania University, 80138, Naples, Italy.
- 3Department of Molecular Biology and Genetics, Izmir Institute of Technology, Izmir, Turkey.
- 4Department of Biology, Faculty of Science, Erciyes University, Kayseri, Turkey.
- 5Department of Medical Genetics, Faculty of Medicine, Erciyes University, Kayseri, Turkey.
- 6Department of Biochemistry, Private Tekden Hospital, Kayseri, Turkey.
- 7Genome and Stem Cell Center, GENKÖK, Erciyes University, Kayseri, Turkey. ozcan@erciyes.edu.tr.
- 8Department of Biology, Faculty of Science, Erciyes University, Kayseri, Turkey. ozcan@erciyes.edu.tr.
- 0Genome and Stem Cell Center, GENKÖK, Erciyes University, Kayseri, Turkey.
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View abstract on PubMed
Summary
This summary is machine-generated.Obesity causes adipose tissue mesenchymal stem cells (MSCs) to senesce, losing stemness and impairing tissue regeneration. This study reveals obesity-induced stress diminishes MSC stemness markers and promotes inflammation.
Area Of Science
- Stem cell biology
- Obesity research
- Tissue regeneration
Background
- Obesity leads to adipose tissue expansion and accumulation of genotoxic stressors.
- These stressors induce oxidative stress, causing senescence in adipose tissue mesenchymal stem cells (MSCs).
- Senescent MSCs lose regenerative potential and secrete factors that promote further senescence, impairing tissue function.
Purpose Of The Study
- To investigate the impact of obesity on the stemness properties of adipose tissue MSCs.
- To determine if obesity-induced stress leads to a loss of stemness markers and impaired regenerative capacity in MSCs.
- To analyze proteomic and gene expression changes in MSCs from obese versus normal-diet mice.
Main Methods
- Cultured MSCs from high-fat diet (obese) and normal diet mice.
- Analyzed stemness-associated gene expression.
- Quantified pluripotent marker (TRA-1-60) expression.
- Performed shotgun proteomic analysis (LC-MS/MS) and bioinformatics evaluation (gene ontology, PPI network).
Main Results
- MSCs from obese mice exhibited a senescent phenotype and altered cell cycle distribution.
- A decline in pluripotent marker expression (TRA-1-60) was observed in obese mice MSCs.
- Gene expression analysis showed decreased stemness markers and increased inflammation/senescence markers in obese MSCs.
- Proteomic analysis confirmed reduced stemness molecules and increased inflammation/senescence markers in obese MSCs.
Conclusions
- Obesity-associated stress conditions cause adipose tissue MSCs to lose their stemness properties.
- This loss of stemness contributes to impaired tissue regeneration in obesity.
- Senescence and inflammation are key mechanisms underlying MSC dysfunction in obese adipose tissue.
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