ArticleCell communication and signaling : CCS2024
Podoplanin depletion in tonsil-derived mesenchymal stem cells induces cellular senescence via regulation of the p16
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Materiobiology-guided regulation of mesenchymal stromal cell fate for aging-related diseases: From basic parameter design to clinical application.Bioactive materials · 2026Review
- The Impact of Large-Scale Expansion on the Functional Properties of Mesenchymal Stem Cells.Stem cell reviews and reports · 2026Review
- Exploring the dual role of extracellular vesicles in coagulation and immune modulation in glioblastoma.Scientific reports · 2026Article
- Mesenchymal stem cell senescence as a potency brake: causes, consequences, and cures.Frontiers in aging · 2026Review
- Magnesium-doped bioactive glass enhances bone regeneration by reversing replicative senescence of human dental pulp stem cells in bone defect therapy.Regenerative biomaterials · 2026Article
- HIF-1α modulates β-catenin pathway to enhance the survival and angiogenesis of PBMSCs under hypoxia environment.World journal of stem cells · 2025Article
- Prematurely Aged Human Microglia Exhibit Impaired Stress Response and Defective Nucleocytoplasmic Shuttling of ALS Associated FUS.Aging cell · 2025Article
- Mesenchymal Stem Cells Senescence: Mechanism and Rejuvenation Interventions.International journal of medical sciences · 2025Review
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Authors and funding
2 authors.
Funding
Abstract
backgroundMesenchymal stem cells (MSCs) are widely used in the development of therapeutic tools in regenerative medicine. However, their quality decreases during in vitro expansion because of heterogeneity and acquired cellular senescence. We investigated the potential role of podoplanin (PDPN) in minimizing cellular senescence and maintaining the stemness of tonsil-derived MSCs (TMSCs).
methodsTMSCs were isolated from human tonsil tissues using an enzymatic method, expanded, and divided into two groups: early-passaged TMSCs, which were cultured for 3-7 passages, and late-passaged TMSCs, which were passaged more than 15 times. The TMSCs were evaluated for cellular senescence and MSC characteristics, and PDPN-positive and -negative cells were identified by fluorescence-activated cell sorting. In addition, MSC features were assessed in siRNA-mediated PDPN-depleted TMSCs.
resultsTMSCs, when passaged more than 15 times and becoming senescent, exhibited reduced proliferative rates, telomere length, pluripotency marker (NANOG, OCT4, and SOX2) expression, and tri-lineage differentiation potential (adipogenesis, chondrogenesis, or osteogenesis) compared to cells passaged less than five times. Furthermore, PDPN protein levels significantly decreased in a passage-dependent manner. PDPN-positive cells maintained their stemness characteristics, such as MSC-specific surface antigen (CD14, CD34, CD45, CD73, CD90, and CD105) and pluripotency marker expression, and exhibited higher tri-lineage differentiation potential than PDPN-negative cells. SiRNA-mediated silencing of PDPN led to decreased cell-cycle progression, proliferation, and migration, indicating the significance of PDPN as a preliminary senescence-related factor. These reductions directly contributed to the induction of cellular senescence via p16
conclusionPDPN may serve as a novel biomarker to mitigate cellular senescence in the clinical application of MSCs.
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