Cellular Senescence |
Request Information |
Cellular senescence is the point at which our cells stop dividing and growing due to damage or lack of necessary components. As cells age, they lose their ability to actively divide and start to undergo senescence.
Senescence refers to a pause in the cell cycle, usually in response to damage. Young senescent cells are presumably cleared by the immune system, but in older tissues, they stick around, secreting harmful proinflammatory signals like IL-6 and IL-8 that damage our bodies further.
As one would guess, the DNA damage and oxidative stress responses, via p53 and AMPK, induce senescence via the retinoblastoma pathway. And telomere shortening causes cells to stop replicating, reinforcing the senescent phenotype.
The cell cycle regulator, p16, plays a still-mysterious role in aging-related senescence. Levels of p16 are more correlated to chronological age than are the levels of any other protein, but its precise regulation in the context of aging is not clear. Developmental signaling, such as by the Id proteins and microRNAs, is involved.
The emerging theme is that it’s not enough to measure one or two biomarkers to unequivocally define the senescent state. To fully characterize aging cells, measure at least a few of the following phenotypic markers: secretory phenotype, beta galactosidase expression, proliferation, heterochromatic foci, flatness of morphology and chromatin alterations.
 Many pathways lead to senescence, and the latest research points to microsRNAs playing a key role. Adapted from Gorospe M, Abdelmehsen K. Micro Regulators come of age in senescence Trends Genet 2011; 27(6).233-41. |
New Publications:
- Salama R, Sadaie M, Hoare M, Narita M. Cellular senescence and its effector programs. Genes Dev. 2014; 28(2):99-114.
- Demaria M, Ohtani N, Youssef SA, Rodier F, Toussaint W, Mitchell JR, Laberge RM, Vijg J, Van Steeg H, Dollé ME, Hoeijmakers JH, de Bruin A, Hara E, Campisi J. An essential role for senescent cells in optimal wound healing through secretion of PDGF-AA. Dev Cell. 2014; 31(6):722-33.
- Ido Y, Duranton A, Lan F, Weikel KA, Breton L, Ruderman NB. Resveratrol Prevents Oxidative Stress-Induced Senescence and Proliferative Dysfunction by Activating the AMPK-FOXO3 Cascade in Cultured Primary Human Keratinocytes. PLoS One. 2015; 10(2):e0115341.
| Featured Technique: Proliferation Assays |
|---|
| Evaluation of cell proliferation is essential for studies of most biological processes and for many cellbased assays. The traditional method for detection of cell proliferation has been the measurement of [3H] thymidine incorporation as cells enter S phase, and subsequent quantification of [3H] thymidine, as performed by scintillation counting. This technology is slow, labor-intensive and has several limitations, including the handling and disposal of radioisotopes and the necessity of expensive equipment. Merck Millipore has developed multiple technologies for biomolecular detection and cellular analysis that offer significant advantages over [3H] thymidine incorporation for quantifying cell proliferation with speed, precision, and accuracy. These include the use of non–radioactive reagents such as EdU, BrdU, WST-1, and MTT. |
| Featured Solution: NEW EdU Cell Proliferation Assays |
|---|
| The use of EdU (5-ethynyl-2’-deoxyuridine) as a thymidine nucleoside analog is a significant improvement compared to the classical BrdU and 3[H] thymidine cell proliferation assays. In contrast to BrdU assay kits, the EdU cell proliferation assays are not antibody based and do not require DNA denaturation for detection of the incorporated nucleoside. Instead, the EdU Cell Proliferation assays measure the incorporation of EdU into newly synthesized DNA with click chemistry for detection by fluorescence microscopy and flow cytometry applications. Features and Benefits
|
| Related Proliferation Assays | ||||
|---|---|---|---|---|
|
| Hallmarks of Aging |
|---|
 Find out how aging may play a role in your research. Learn more! Visit Hallmarks of Aging Home Page. |