Evidence map›Paper›PMID 38185703›Full record

ArticleStem cell research & therapy2024

Uncovering impaired mitochondrial and lysosomal function in adipose-derived stem cells from obese individuals with altered biological activity.

Bo Wang, Ge Zhang, Yuwen Hu, Ali Mohsin, Zhimin Chen, Weijie Hao, Zhanxia Li, Wei-Qiang Gao, Meijin Guo, Huiming Xu

Abstract read
PubMed Full text at PMC Publisher
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Article in Stem cell research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 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

10 authors.

Bo WangState Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, 130 Meilong Rd., P.O. Box 329#, Shanghai, 200237, People's Republic of China.
Ge ZhangState Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, 130 Meilong Rd., P.O. Box 329#, Shanghai, 200237, People's Republic of China.
Yuwen HuState Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, 130 Meilong Rd., P.O. Box 329#, Shanghai, 200237, People's Republic of China.
Ali MohsinState Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, 130 Meilong Rd., P.O. Box 329#, Shanghai, 200237, People's Republic of China.
Zhimin ChenState Key Laboratory of Oncogenes and Related Genes, and Renji-MedX Clinical Stem Cell Research Center RenJi Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, People's Republic of China.
Weijie HaoState Key Laboratory of Oncogenes and Related Genes, and Renji-MedX Clinical Stem Cell Research Center RenJi Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, People's Republic of China.
Zhanxia LiDepartment of Respiratory Medicine, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 600 Yishan Road, Xuhui District, Shanghai, 200235, People's Republic of China. zhanxia-li@hotmail.com.
Wei-Qiang GaoState Key Laboratory of Oncogenes and Related Genes, and Renji-MedX Clinical Stem Cell Research Center RenJi Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, People's Republic of China. gao.weiqiang@sjtu.edu.cn.
Meijin GuoState Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, 130 Meilong Rd., P.O. Box 329#, Shanghai, 200237, People's Republic of China. guo_mj@ecust.edu.cn.ORCID 0000-0002-3171-4802
Huiming XuState Key Laboratory of Oncogenes and Related Genes, and Renji-MedX Clinical Stem Cell Research Center RenJi Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, People's Republic of China. quxuhm123@163.com.

Funding

111 Project B18022Fundamental Research Funds for the Central Universities 22221817014Fundamental Research Funds for the Central Universities Nos. 22221818014National Natural Science Foundation of China 81373286National Natural Science Foundation of China No. 22250410275Strategic Priority Research Program of the Chinese Academy of Sciences No. XDA16030702
6 · The paper itself

Abstract

backgroundAdipose-derived stem cells (ADSCs) have been extensively used in preclinical and clinical trials for treating various diseases. However, the differences between ADSCs from lean individuals (L-ADSCs) and those from obese individuals (O-ADSCs) have not been thoroughly investigated, particularly regarding their mitochondrial and lysosomal functions. Therefore, this study aims to evaluate the differences between L-ADSCs and O-ADSCs in terms of cell biological activity, mitochondria, and lysosomes.

methodsWe first isolated and cultured L-ADSCs and O-ADSCs. We then compared the differences between the two groups in terms of biological activity, including cell proliferation, differentiation potential, and their effect on the polarization of macrophages. Additionally, we observed the mitochondrial and lysosomal morphology of ADSCs using an electronic microscope, MitoTracker Red, and lysotracker Red dyes. We assessed mitochondrial function by examining mitochondrial membrane potential and membrane fluidity, antioxidative ability, and cell energy metabolism. Lysosomal function was evaluated by measuring autophagy and phagocytosis. Finally, we performed transcriptome analysis of the ADSCs using RNA sequencing.

resultsThe biological activities of O-ADSCs were decreased, including cell immunophenotypic profiles, cell proliferation, and differentiation potential. Furthermore, compared to L-ADSCs, O-ADSCs promoted M1-type macrophage polarization and inhibited M2-type macrophage polarization. Additionally, the mitochondrial morphology of O-ADSCs was altered, with the size of the cells becoming smaller and mitochondrial fragments increasing. O-ADSCs also exhibited decreased mitochondrial membrane potential and membrane fluidity, antioxidative ability, and energy metabolism. With respect to lysosomes, O-ADSCs contained ungraded materials in their lysosomes, enhanced lysosomal permeability, and reduced autophagy and phagocytosis ability. RNA sequence analysis indicated that the signalling pathways related to cell senescence, cancer, and inflammation were upregulated, whereas the signalling pathways associated with stemness, cell differentiation, metabolism, and response to stress and stimuli were downregulated.

conclusionsThis study indicates that ADSCs from individuals (BMI > 30 kg/m

Indexed as

LysosomesObesityAdiposityAntioxidantsHumansPhagocytosisStem CellsAntioxidantsAdipose-derived stem cellsLysosomal dysfunctionMitochondrial dysfunctionObesity

Identifiers

PMID38185703
PMCPMC10773039

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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.