Senescence Map Selection Guide

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-βGal	Cellular Senescence Plate Assay Kit - SPiDER-βGal	DNA Damage Detection Kit – γH2AX *Please Contact Us	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-β-gal activity	SA-β-gal activity	Changes in DNA Damage	Changes in the Nucleolus
Detection method	Imaging Substrate: SPiDER-βGal	Plate Assay Substrate: SPiDER-βGal	Imaging Detection of γH2AX 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#	SG03	SG05	Green: G265 / Red:G266 Deep Red: G267	Green: N511 / Red: N512

Feature of Cellular Senescence

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.

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.