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Related Concept Videos

Replicative Cell Senescence02:15

Replicative Cell Senescence

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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
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Related Experiment Video

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Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

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Techniques to Induce and Quantify Cellular Senescence.

Nicole Noren Hooten1, Michele K Evans2

  • 1Laboratory of Epidemiology and Population Science, National Institute on Aging, National Institutes of Health; norenhootenn@mail.nih.gov.

Journal of Visualized Experiments : Jove
|May 19, 2017
PubMed
Summary
This summary is machine-generated.

Cellular senescence is a state of long-term cell-cycle arrest induced by stress. This study details methods to induce and monitor senescence, crucial for understanding aging and tissue repair.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Aging Research

Background:

  • Cellular senescence is a protective mechanism against damage, leading to cell-cycle arrest.
  • Senescent cells accumulate with age and influence development, repair, and disease.
  • Key hallmarks include SA-β-gal, altered protein levels (p16INK4A, p53, p21), DNA damage (γ-H2AX), SAHF, and SASP.

Purpose of the Study:

  • To provide standardized protocols for inducing replicative and DNA damage-induced senescence.
  • To present methods for monitoring senescence using established markers.
  • To enable quantification of cell cycle regulators and SASP factors.

Main Methods:

  • Induction of senescence via replicative exhaustion and DNA damage.
  • Assessment of senescence-associated β-galactosidase (SA-β-gal) activity.
  • Staining for DNA damage marker γ-H2AX and Senescence-associated Heterochromatin Foci (SAHF).
  • Quantification of cell cycle regulator and SASP factor mRNA and protein levels.

Main Results:

  • Established protocols for inducing two major types of cellular senescence.
  • Demonstrated utility of SA-β-gal, γ-H2AX, and SAHF as reliable senescence markers.
  • Validated methods for quantifying key molecular players in senescence.

Conclusions:

  • The described protocols and techniques facilitate robust assessment of cellular senescence.
  • These methods are applicable across diverse experimental models and tissues.
  • This work supports further research into the roles of senescence in health and disease.