Oxygen sensitivity severely limits the replicative lifespan of murine fibroblasts

By S. Parrinello, Enrique Samper, A. Krtolica, J. Goldstein, S. Melov, J. Campisi. Nature Cell Biology, 2003

1,155 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/8c3c0e8073ba20e9bcfdf81f1bfd7951f27194c3

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. J. Campisi
2. Jesús Gil
3. M. Demaria
4. Manuel Serrano
5. Adam Freund
6. Stephen P. Jackson
7. F. d’Adda di Fagagna
8. Zhijian J. Chen

In Physiology

1. J. Campisi
2. Jesús Gil
3. M. Demaria
4. Manuel Serrano
5. Adam Freund
6. Jean-Philippe Coppé
7. Zhijian J. Chen
8. M. Blasco

Citations in the corpus

• Glycolytic enzymes can modulate cellular life span. (2005, background): “essentially immortal and show less oxidative DNA damage if propagated in 3% oxygen (13).”
• The essence of senescence. (2010, background): “Senescence of MEFs can be bypassed also by inactivation of p53 or simultaneous ablation of RB family genes (Tanaka et al. 1994; Dannenberg et al. 2000; Sage et al. 2000).”
• The signals and pathways activating cellular senescence. (2005, background): “Oxidative stress can cause DNA damage and also accelerate telomere shortening rates (von Zglinicki, Saretzki, Docke, & Lotze, 1995; Forsyth et al., 2003; Parrinello et al., 2003).”
• Aging, Cellular Senescence, and Cancer (2012, background): “This finding may be complicated by the fact that the proliferative arrest of mouse cells cultured in ambient oxygen concentrations (approximately 20%), which is substantially higher than the oxygen concentrations to which cells are exposed in vivo, has only some features of the senescence response t”
• A DNA damage checkpoint response in telomere-initiated senescence (2003, background): “Conversely, it might help to explain why certain DNA-repair-deficient knockout mice and human cell lines senesce prematurel”
• cGAS is essential for cellular senescence (2017, methodology): “A commonly used method to detect senescence cells is SA-β-Gal staining (28).”
• Stromal-epithelial interactions in aging and cancer: senescent fibroblasts alter epithelial cell differentiation (2004, methodology): “Mouse mammary fibroblasts (mBF) and mammary epithelial organoids were isolated from 3- to 4-month-old virgin C57Bl/6 mice and cultured as described previously (Simian et al., 2001), with the exception that they were cultured in a 3% oxygen atmosphere (Parrinello et al., 2003).”
• Four faces of cellular senescence (2011, neutral): “, tissue culture plastic), serum (most cells experience plasma, not serum, in vivo), and oxidative stress (e.g., culture in atmospheric O2, which is hyperphysiological; Fusenig and Boukamp, 1998; Yaswen and Stampfer, 2002; Parrinello et al., 2003).”
• Senescence impairs successful reprogramming to pluripotent stem cells. (2009, background): “In particular, it has been shown that DNA damage caused by oxidative stress is the main cause of senescence onset in murine cells (Parrinello et al., 2003).”
• Repair and genetic consequences of endogenous DNA base damage in mammalian cells. (2004, background): “Moreover, differences in oxygen sensitivity of cells in culture (116) do not appear to correlate with observed cancer rates in mice versus humans deficient specifically in the repair of oxidative DNA base damage.”
• Akt determines replicative senescence and oxidative or oncogenic premature senescence and sensitizes cells to oxidative apoptosis (2008, background): “Akt Regulates Cellular Life Span and Intracellular ROS Levels by Mediating Oxygen Consumption and Inhibiting FoxO Transcription Factors Life span in culture of MEFs, and to some extent HDFs, is coupled to oxygen consumption and intracellular ROS (Parrinello et al., 2003).”
• Cellular senescence in cancer and aging. (2007, positive): “Early studies using in vitro cultured cells showed that the infliction of various forms of DNA damage triggers senescence (Parrinello et al., 2003; te Poele et al., 2002).”
• Lamin B1 loss is a senescence-associated biomarker (2012, background): “, arrested growth, SA-βgal expression) but not all features (e.g., loss of c-FOS inducibility, the SASP; Parrinello et al., 2003; Coppe et al., 2010).”