“Senescent Cell Detection – Selection Guide”


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

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.


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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.




Sample Senescence induction Senescence Marker Factor involved in senescence Citation
IMR90
(human lung fibroblast cell)
passage of aging SA-ßGal
p16, p21
enlarged nucleoli
SETD8 expression
H4K20me1
mitochondrial oxidative phosphorylation
ribosome biogenesis
SETD8 (methyltransferase) low expression mitochondrial oxidative phosphorylation
ribosome biogenesis
Aged satellite cells - SA-ßGal
p16
Autophagy activity
ROS
Mitochondria membrane potential
Atg7-deficient satellite cells Inhibition of autophagy SA-ßGal
P15, p16, p21
γ-H2AX
ROS
Mitochondria membrane potential
Fibroblasts from patients with type 2 diabetes - SA-ßGal
p21, p53
γ-H2AX
NADPH / NADP
(resistance to oxidative stress )
NADPH oxidase
(ROS )
IMR90 Ethidium Bromide (depletion of mtDNA) + pyruvate withdrawal SA-ßGal NAD+ / NADH
MDA-MB-231
(human breast cancer cells)
Radiation-induced senescence +
low expression of securin
SA-ßGal Lactate
LDH activity
(glycolysis )
MEF
(mouse embryonic fibroblasts)
overexpression of cancer gene passage of aging overexpression of transcription factor(E2F1) SA-ßGal
p16, p21
enlarged nucleoli
Ribosome RNA
p53
Mouse tail-tip fibroblasts 2 month-old WT,
22 month-old WT,
p16 KO(22 month-old)
SA-ßGal
p14, p16
NAD+
SIRT3



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.