Cellular senescence, the irreversible state of cell-cycle arrest, can be induced by various cellular stresses. Here, we describe protocols to induce cellular senescence and methods to assess markers of senescence.
A subscription to JoVE is required to view this content. Sign in or start your free trial.
Method Article
Cellular senescence, the irreversible state of cell-cycle arrest, can be induced by various cellular stresses. Here, we describe protocols to induce cellular senescence and methods to assess markers of senescence.
In response to cellular stress or damage, proliferating cells can induce a specific program that initiates a state of long-term cell-cycle arrest, termed cellular senescence. Accumulation of senescent cells occurs with organismal aging and through continual culturing in vitro. Senescent cells influence many biological processes, including embryonic development, tissue repair and regeneration, tumor suppression, and aging. Hallmarks of senescent cells include, but are not limited to, increased senescence-associated β-galactosidase activity (SA-β-gal); p16INK4A, p53, and p21 levels; higher levels of DNA damage, including γ-H2AX; the formation of Senescence-associated Heterochromatin Foci (SAHF); and the acquisition of a Senescence-associated Secretory Phenotype (SASP), a phenomenon characterized by the secretion of a number of pro-inflammatory cytokines and signaling molecules. Here, we describe protocols for both replicative and DNA damage-induced senescence in cultured cells. In addition, we highlight techniques to monitor the senescent phenotype using several senescence-associated markers, including SA-β-gal, γ-H2AX and SAHF staining, and to quantify protein and mRNA levels of cell cycle regulators and SASP factors. These methods can be applied to the assessment of senescence in various models and tissues.
Over half a century ago, Hayflick and colleagues described how untransformed cells proliferate in culture, but for only a finite period of time1. Long-term culturing of human fibroblasts caused the cells to stop proliferating; however, they were metabolically active, and this was called cellular senescence. Senescence can be beneficial for inhibiting tumorigenesis, but it also can be detrimental, as it is thought to contribute to the loss of regenerative capacity that occurs with aging2,3. Senescent cells have been shown to accumulate in tissues as humans age4 an....
Access restricted. Please log in or start a trial to view this content.
1. Inducing Replicative Senescence
Access restricted. Please log in or start a trial to view this content.
Figures 2 - 6 show representative results from SA-β-gal staining; staining for γ-H2AX and SAHF; assessment of protein levels of p16INK4A, p21, and p53; and mRNA and protein levels of senescent-associated molecules. Increased SA-β-gal staining occurs with replicative and DNA damage-induced senescence. Also, observe the morphological changes that occur with senescence. Cells become enlarged and flat compared to the spindle appearance of proliferating fibroblasts........
Access restricted. Please log in or start a trial to view this content.
Here, we have described methods for replicative and DNA-damage induced senescence using human diploid fibroblasts. In addition, techniques for quantifying protein and mRNA levels of various senescence-associated proteins are included, as well as staining for SA-β-gal and for the DNA-damage marker γ-H2AX. These protocols can be widely used to assess senescent phenotypes both in vitro and in vivo, although many caveats exist for characterizing senescence in vivo20
Access restricted. Please log in or start a trial to view this content.
The authors have nothing to disclose.
This study was supported by the Intramural Research Program of the National Institutes of Health, National Institute on Aging. The authors wish to thank Myriam Gorospe and Kotb Abdelmohsen for many helpful discussions about senescence and Kotb Abdelmohsen for also critically reading the manuscript. We also thank our laboratory members, especially Douglas Dluzen for critically reading the manuscript.
....Access restricted. Please log in or start a trial to view this content.
| Name | Company | Catalog Number | Comments |
|---|---|---|---|
| 16% Tris-glycine gels | Invitrogen | XP00160BOX | |
| Acid-Phenol ChCl3 | Ambion | AM9720 | |
| Alexa-Fluor 568 goat anti-mouse antibody | Invitrogen | A11031 | 1:300 dilution |
| Cell lifters | Corning Inc. | 3008 | Cell scraper |
| ECL anti-mouse HRP linked antibody | Amersham | NA931V | |
| ECL Plus Western Blotting Substrate | Pierce | 32132 | ECL |
| DAPI | Molecular Probes | MP01306 | stock 5 mg/mL in dH2O |
| GAPDH antibody | Santa Cruz | sc-32233 | 1:1,000 - 5,000 dilution |
| GlycoBlue | Ambion | AM9515 | |
| Histone H3 dimethyl K9 monoclonal antibody | Abcam | 1220 | 1:500 dilution |
| Human IL-6 Quantikine ELISA assay | R&D systems | D6050 | |
| Human IL-8 Quantikine ELISA assay | R&D systems | D8000C | |
| Human GROa Quantikine ELISA assay | R&D systems | DRG00 | |
| N-N-dimethylformamide | Sigma | D4551 | DMF |
| p16 monoclonal antibody | BD Biosciences | 51-1325gr | 1:500 dilution |
| p21 monoclonal antibody | Millipore | 05-345 | 1:750 dilution |
| p53 monoclonal antibody | Santa Cruz | sc-126 | 1:500 dilution clone DO-1 |
| phospho-H2AX (Ser139) FITC conjugate antibody | Cell Signaling | 9719 | 1:2,000 dilution |
| POWER SYBR-green PCR master mix | Applied Biosystems | 4367659 | |
| Pre-stained molecular weight markers | Biorad | 161-0374 | |
| ProLong Gold Antifade | Invitrogen | P36930 | |
| PVDF membrane | Thermo Scientific | 88518 | |
| Senescence β-Galactosidase Staining Kit | Cell Signaling | 9860 | |
| TRIzol | Ambion/Life Tech | 10296028 |
Access restricted. Please log in or start a trial to view this content.