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|
|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|
|Imaging Detection of γH2AX by secondary antibody method||Imaging Detection of the Nucleolus by RNA staining reagent|
|Plate reader||Fluorescence microscopy||Fluorescence microscopy|
|Sample||Live cells Fixed cells||Live cells|
(lysis of live cells)
|Fixed cells||Fixed cells|
Deep Red: G267
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.
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.