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Characterization of transcriptional landscape in bone marrow-derived mesenchymal stromal cells treated with aspirin by RNA-seq
Author(s) -
Xinpeng Liu,
Yuanbo Zhan,
Wenxia Xu,
Lixue Liu,
Xiaoyao Liu,
Junlong Da,
Kai Zhang,
Xinjian Zhang,
Jianqun Wang,
Ziqi Liu,
Han Jin,
Bin Zhang,
Ying Li
Publication year - 2022
Publication title -
peerj
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.927
H-Index - 70
ISSN - 2167-8359
DOI - 10.7717/peerj.12819
Subject(s) - mesenchymal stem cell , aspirin , senescence , bone marrow , western blot , immune system , stromal cell , biology , downregulation and upregulation , progenitor cell , cancer research , stem cell , medicine , immunology , microbiology and biotechnology , biochemistry , gene
Aspirin is a common antipyretic, analgesic, and anti-inflammatory drug, which has been reported to extend life in animal models and application in the treatment of aging-related diseases. However, it remains unclear about the effects of aspirin on bone marrow-derived mesenchymal stromal cells (BM-MSCs). Here, we aimed to analyze the influence of aspirin on senescence and young BM-MSCs. Methods BM-MSCs were serially passaged to construct a replicative senescence model. SA-β-gal staining, PCR, western blot, and RNA-sequencing were performed on BM-MSCs with or without aspirin treatment, to examine aspirin’s impact on bone marrow-derived mesenchymal stem cells. Results SA-β-gal staining, PCR, and western blot revealed that aspirin could alleviate the cellular expression of senescence-related indicators of BM-MSCs, including a decrease of SA-β-gal-positive cells and staining intensity, and downregulation of p16, p21, and p53 expression after aspirin treatment. RNA-sequencing results shown in the biological processes related to aging, aspirin could influence cellular immune response and lipid metabolism. Conclusion The efficacy of aspirin for retarding senescence of BM-MSCs was demonstrated. Our study indicated that the mechanisms of this delay might involve influencing immune response and lipid metabolism.

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