Cellular Senescence Detection Comparison
Cellular senescence is considered crucial to many different research areas, especially since the recent discovery of the senescence-associated secretory phenotype (SASP). SASP is a known risk factor for malignant transformation and exploration into stem cell research has found a link between SASP and the aging phenomenon. The features of cellular senescence were summarized based on modern publications that have a high number of citations.
Various Senescent Cell from Various Indicators
| Product | Cellular Senescence Detection Kit – SPiDER-ßGal | Cellular Senescence Plate Assay Kit – SPiDER-ßGal | DNA Damage Detection Kit – γH2AX * Coming Soon | Nucleolus Bright Green / Red |
|---|---|---|---|---|
| Detection | Fluorescence | Fluorescence | Fluorescence | Fluorescence |
| Wavelength (Ex/Em) | 500 – 540 nm / 530 – 570 nm | 535 nm / 580 nm | Green: 494 nm / 518 nm Red: 550 nm / 566 nm Deep Red: 646 nm / 668 nm | Green: 513 nm / 538 nm Red: 537 nm / 605 nm |
| Indicator | SA-ß-gal activity | SA-ß-gal activity | Changes in DNA damage | Changes in the Nucleolus |
| Detection method | Imaging Substrate:SPiDER-ßGal | Plate assay Substrate:SPiDER-ßGal | Imaging Detection of γH2AX by secondary antibody method | Imaging Detection of the Nucleolus by RNA staining reagent |
| Instrument | Fluorescence microscopy Flow cytometry | Plate reader | Fluorescence microscopy | Fluorescence microscopy |
| Sample | Live cells Fixed cells | Live cells (lysis of live cells) | Fixed cells | Fixed cells |
| data |  |  |  |  |
| Item# | SG04 | SG05 | Green: G265 Red: G266 Deep Red: G267 | Green: N511 Red: N512 |
Feature of Cellular Senescence
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Evaluate senescent cells from various makers
In WI-38 cells at different passages SA-ß-Gal activity, mitochondrial membrane potential, and cellular metabolism (Glucose and Lactate) were evaluated using each specific kit. In senescent cells, SA-ß-Gal activity was enhanced and mitochondrial membrane potential was reduced. Consumption of Glucose and lactate level in the supernatant measured as an indicator of metabolism was increased.
Publications
①
H. Tanaka, S. Takebayashi, A. Sakamoto, N. Saitoh, S. Hino and M. Nakao, “The SETD8/PR-Set7 Methyltransferase Functions as a Barrier to Prevent Senescence-Associated Metabolic Remodeling.”, Cell Reports, 2017, 18(9), 2148.
②
L. Garcia-Prat, M. Martinez-Vicente and P. Munoz-Canoves, “Autophagy: a decisive process for stemness”, Oncotarget, 2016, 7(11), 12286.
③
M. Bitar, S. Abdel-Halim and F. Al-Mulla, “Caveolin-1/PTRF upregulation constitutes a mechanism for mediating p53-induced cellular senescence: implications for evidence-based therapy of delayed wound healing in diabetes”, Am J Physiol Endocrinol Metab., 2013, 305(8), E951.
④
C. Wiley, M. Velarde, P. Lecot, A. Gerencser, E. Verdin, J. Campisi, et. al., “Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype”, Cell Metab., 2016, 23(2), 303.
⑤
E. Liao, Y. Hsu, Q. Chuah, Y. Lee, J. Hu, T. Huang, P-M Yang & S-J Chiu, “Radiation induces senescence and a bystander effect through metabolic alterations.”, Cell Death Dis., 2014, 5, e1255.
⑥
K. Nishimura, T. Kumazawa, T. Kuroda, A. Murayama, J. Yanagisawa and K. Kimura, “Perturbation of Ribosome Biogenesis Drives Cells into Senescence through 5S RNP-Mediated p53 Activation”, Cell Rep. 2015, 10(8), 1310.
⑦
M. J. Son, Y. Kwon, T. Son and Y. S. Cho, “Restoration of Mitochondrial NAD+ Levels Delays Stem Cell Senescence and Facilitates Reprogramming of Aged Somatic Cells”, Stem Cells. 2016, 34(12), 2840.