ArticleCell stress & chaperones2014
Lipocalin 2 decreases senescence of bone marrow-derived mesenchymal stem cells under sub-lethal doses of oxidative stress.
Article in Cell stress & chaperones, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- USP22 alleviates oxidative stress-induced BMSCs senescence by stabilizing SPI1 protein.Molecular genetics and genomics : MGG · 2026Article
- Understanding the molecular basis of mesenchymal stem cell stemness: implications for clinical applications.Cell death & disease · 2025Review
- Review
- Immuno-activated mesenchymal stem cell living electrospun nanofibers for promoting diabetic wound repair.Journal of nanobiotechnology · 2022Article
- Lipocalin 2 serum levels correlate with age and bone turnover biomarkers in healthy subjects but not in postmenopausal osteoporotic women.Bone reports · 2021Article
- Dynamic Changes of the Bone Marrow Niche: Mesenchymal Stromal Cells and Their Progeny During Aging and Leukemia.Frontiers in cell and developmental biology · 2021Review
- Implication and role of neutrophil gelatinase-associated lipocalin in cancer: lipocalin-2 as a potential novel emerging comprehensive therapeutic target for a variety of cancer types.Molecular biology reports · 2020Review
- Downregulation of MicroRNA-206 Alleviates the Sublethal Oxidative Stress-Induced Premature Senescence and Dysfunction in Mesenchymal Stem Cells via Targeting Alpl.Oxidative medicine and cellular longevity · 2020Article
- A revealing review of mesenchymal stem cells therapy, clinical perspectives and Modification strategies.Stem cell investigation · 2019Review
- Serum-mediated Activation of Bone Marrow-derived Mesenchymal Stem Cells in Ischemic Stroke Patients: A Novel Preconditioning Method.Cell transplantation · 2018Article
- Ectopic Expression of Innate Immune Protein, Lipocalin-2, in Lactococcus lactis Protects Against Gut and Environmental Stressors.Inflammatory bowel diseases · 2017Article
- Identification of Bone Marrow-Derived Soluble Factors Regulating Human Mesenchymal Stem Cells for Bone Regeneration.Stem cell reports · 2017Article
- Environmental preconditioning rejuvenates adult stem cells' proliferation and chondrogenic potential.Biomaterials · 2017Review
- Genetic Engineering of Mesenchymal Stem Cells to Induce Their Migration and Survival.Stem cells international · 2016Review
- Stanniocalcin 2 enhances mesenchymal stem cell survival by suppressing oxidative stress.BMB reports · 2015Article
- The Lcn2-engineered HEK-293 cells show senescence under stressful condition.Iranian journal of basic medical sciences · 2015Article
- In vitro augmentation of mesenchymal stem cells viability in stressful microenvironments : In vitro augmentation of mesenchymal stem cells viability.Cell stress & chaperones · 2015Review
- Lipocalin-2 enhances angiogenesis in rat brain endothelial cells via reactive oxygen species and iron-dependent mechanisms.Journal of neurochemistry · 2015Article
- Nucleofection optimization and in vitro anti-tumourigenic effect of TRAIL-expressing human adipose-derived mesenchymal stromal cells.Cancer cell international · 2014Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The regenerative potential of mesenchymal stem cells (MSCs) is impaired by cellular senescence, a multi factorial process that has various functions. However, pathways and molecules involved in senescence have not been fully identified. Lipocalin 2 (Lcn2) has been the subject of intensive research, due to its contribution to many physiological and pathophysiological conditions. The implication of Lcn2 has been reported in many conditions where senescence also occurs. In the present study, we evaluated the role of Lcn2 in the occurrence of senescence in human bone marrow-derived mesenchymal stem cells (hB-MSCs) under oxidative conditions. When hB-MSCs were genetically engineered to over-express Lcn2 (MSC-Lcn2) and exposed to H2O2, the proliferation rate of the cells increased. However, the number of colonies and the number of cells that made up each colony in both MSC-V and MSC-Lcn2 cells decreased compared to those cultivated under normal conditions. Our results revealed that over-expression of recombinant Lcn2 in hB-MSCs decreases senescence induced by H2O2 treatment. Senescent cells were observed in aged hB-MSCs; however, no alteration in the expression level of Lcn2 was detected compared to earlier passages. Finally, a higher amount of Lcn2 protein was detected in the plasma of the elderly than in young people. Our findings suggest that Lcn2 might restore the health and regeneration potential of MSCs by decreasing senescence.
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