ArticleStem cell research & therapy2017
Decoy TRAIL receptor CD264: a cell surface marker of cellular aging for human bone marrow-derived mesenchymal stem cells.
Article in Stem cell research & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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Who cites it
25 citing papers in PubMed, 49 citations in OpenAlex.
- Chimeric Antigen Receptor T Cells as Living Therapeutics Targeting Senescence and Age-Related Diseases.Research (Washington, D.C.) · 2026Review
- Dexamethasone-boosted mesenchymal stem cell secretome: insight into hepatic protection.BMC biotechnology · 2025Article
- RNA sequencing identifiesCytotechnology · 2025Article
- Mesenchymal Stem Cells Senescence: Mechanism and Rejuvenation Interventions.International journal of medical sciences · 2025Review
- Drug Delivery Strategies for Age-Related Diseases.International journal of molecular sciences · 2024Review
- Podoplanin depletion in tonsil-derived mesenchymal stem cells induces cellular senescence via regulation of the p16Cell communication and signaling : CCS · 2024Article
- Unveiling heterogeneity in MSCs: exploring marker-based strategies for defining MSC subpopulations.Journal of translational medicine · 2024Review
- CD317Stem cell research & therapy · 2024Article
- Reliable Hallmarks and Biomarkers of Senescent Lymphocytes.International journal of molecular sciences · 2023Review
- Studying Hepatic Stellate Cell Senescence.Methods in molecular biology (Clifton, N.J.) · 2023Review
- Why stem/progenitor cells lose their regenerative potential.World journal of stem cells · 2021Review
- Review
- Single-cell RNA sequencing deconvolutes theInternational journal of biological sciences · 2021Article
- CD26 Inhibition Potentiates the Therapeutic Effects of Human Umbilical Cord Blood-Derived Mesenchymal Stem Cells by Delaying Cellular Senescence.Frontiers in cell and developmental biology · 2021Article
- Role of Hyperglycemia in the Senescence of Mesenchymal Stem Cells.Frontiers in cell and developmental biology · 2021Review
- Positively Correlated CD47 Activation and Autophagy in Umbilical Cord Blood-Derived Mesenchymal Stem Cells during Senescence.Stem cells international · 2021Article
- Article
- Human Induced Pluripotent Stem Cell-Derived Mesenchymal Stem Cells Acquire Rejuvenation and Reduced Heterogeneity.Frontiers in cell and developmental biology · 2021Review
- Senescent mesenchymal stem/stromal cells and restoring their cellular functions.World journal of stem cells · 2020Review
- A cautionary tale about the use of colony-forming efficiency as a proxy for the survival of mesenchymal stem cells.Stem cell research & therapy · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMesenchymal stem cells (MSCs) are a mixture of progenitors that are heterogeneous in their regenerative potential. Development of MSC therapies with consistent efficacy is hindered by the absence of an immunophenotype of MSC heterogeneity. This study evaluates decoy TRAIL receptor CD264 as potentially the first surface marker to detect cellular aging in heterogeneous MSC cultures.
methodsCD264 surface expression, regenerative potential, and metrics of cellular aging were assessed in vitro for marrow MSCs from 12 donors ages 20-60 years old. Male and female donors were age matched. Expression of CD264 was compared with that of p16, p21, and p53 during serial passage of MSCs.
resultsWhen CD264
conclusionsThese results suggest that CD264 is a surface marker of cellular age for MSCs, not the chronological age of the MSC donor. CD264 is first upregulated in MSCs at an intermediate stage of cellular aging and remains upregulated as aging progresses towards senescence. The strong inverse correlation of CD264
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Registered trials
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.