ArticleStem cells (Dayton, Ohio)2013
Cell autonomous and nonautonomous mechanisms drive hematopoietic stem/progenitor cell loss in the absence of DNA repair.
Article in Stem cells (Dayton, Ohio), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Reactive Oxygen Species in Cardiovascular and Hematological Diseases: Mechanisms and Therapeutic Strategies.Cureus · 2026Review
- Loss of SYNCRIP unleashes APOBEC-driven mutagenesis, tumor heterogeneity, and AR-targeted therapy resistance in prostate cancer.Cancer cell · 2023Article
- Reduction of senescent fibro-adipogenic progenitors in progeria-aged muscle by senolytics rescues the function of muscle stem cells.Journal of cachexia, sarcopenia and muscle · 2022Article
- ATR activity controls stem cell quiescence via the cyclin F-SCF complex.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Article
- Nervous System-Systemic Crosstalk in SARS-CoV-2/COVID-19: A Unique Dyshomeostasis Syndrome.Frontiers in neuroscience · 2021Review
- SOX2 and p53 Expression Control Converges in PI3K/AKT Signaling with Versatile Implications for Stemness and Cancer.International journal of molecular sciences · 2020Review
- XPF-ERCC1 protects liver, kidney and blood homeostasis outside the canonical excision repair pathways.PLoS genetics · 2020Article
- DNA damage in aging, the stem cell perspective.Human genetics · 2020Review
- Rapamycin Rescues Age-Related Changes in Muscle-Derived Stem/Progenitor Cells from Progeroid Mice.Molecular therapy. Methods & clinical development · 2019Article
- mTOR signaling plays a critical role in the defects observed in muscle-derived stem/progenitor cells isolated from a murine model of accelerated aging.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2017Article
- Supplementation withFrontiers in immunology · 2016Article
- Mitochondrial ATP transporter Ant2 depletion impairs erythropoiesis and B lymphopoiesis.Cell death and differentiation · 2015Article
- Concise review: hematopoietic stem cell aging and the prospects for rejuvenation.Stem cells translational medicine · 2015Review
- Stem cells: the pursuit of genomic stability.International journal of molecular sciences · 2014Review
- Quiescent hematopoietic stem cells accumulate DNA damage during aging that is repaired upon entry into cell cycle.Cell stem cell · 2014Article
- Purinergic P2Y₁₄ receptor modulates stress-induced hematopoietic stem/progenitor cell senescence.The Journal of clinical investigation · 2014Article
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Authors and funding
5 authors.
Funding
Abstract
Daily, cells incur tens of thousands of DNA lesions caused by endogenous processes. Due to their long-lived nature, adult stem cells may be particularly susceptible to the negative impact of this constant genotoxic stress. Indeed, in murine models of DNA repair deficiencies, there is accumulation of DNA damage in hematopoietic stem cells and premature loss of function. Herein, we demonstrate that mice expressing reduced levels of ERCC1-XPF DNA repair endonuclease (Ercc1-/Δ mice) spontaneously display a progressive decline in the number and function of hematopoietic stem/progenitor cells (HSPCs). This was accompanied by increased cell death, expression of senescence markers, reactive oxygen species, and DNA damage in HSPC populations, illustrating cell autonomous mechanisms that contribute to loss of function. In addition, the bone marrow microenvironment of Ercc1-/Δ mice was not permissive for the engraftment of transplanted normal stem cells. Bones from Ercc1-/Δ mice displayed excessive osteoclastic activity, which alters the microenvironment in a way that is unfavorable to HSPC maintenance. This was accompanied by increased proinflammatory cytokines in the bone marrow of Ercc1-/Δ mice. These data provide novel evidence that spontaneous, endogenous DNA damage, if not repaired, promotes progressive attrition of adult stem cells via both cell autonomous and nonautonomous mechanisms.
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