Related Experiment Video

Updated: May 21, 2026

Development and Application of Rapamycin-regulated Tyrosine Phosphatases
06:56

Development and Application of Rapamycin-regulated Tyrosine Phosphatases

Published on: September 6, 2024

Suppression of replicative senescence by rapamycin in rodent embryonic cells

Tatiana V Pospelova1, Olga V Leontieva, Tatiana V Bykova

  • 1Institute of Cytology, St. Petersburg, Russia. tvpgroup@mail.ru

Cell Cycle (Georgetown, Tex.)
|June 8, 2012
PubMed

Insights

Rapamycin partially suppresses cellular senescence in rodent cells by inhibiting the target of rapamycin (TOR) pathway. While it slows aging, it also causes cell cycle arrest, requiring careful dosage to avoid quiescence.

Area of Science:

  • Cell Biology
  • Aging Research
  • Molecular Biology

Background:

  • The target of rapamycin (TOR) pathway plays a role in aging across species.
  • Previous studies showed mTOR promotes stress-induced senescence (geroconversion), while rapamycin inhibits it.
  • This study explores rapamycin's effect on replicative senescence in rodent cells.

Purpose of the Study:

  • To investigate if rapamycin can suppress replicative senescence in rodent cells.
  • To determine the efficacy and potential side effects of rapamycin on cellular aging.
  • To understand the balance between gerosuppression and cytostasis induced by rapamycin.

Main Methods:

  • Treatment of mouse embryonic fibroblasts (MEFs) and rat embryonic fibroblasts (REFs) with varying concentrations of rapamycin.
  • Monitoring of cellular morphology, proliferation rates, and senescence markers (SA-β-Gal, pS6, γH2AX/53BP1 foci).
  • Analysis of rapamycin's inhibitory concentration (IC50) for proliferation and its effect on pS6 phosphorylation.

Main Results:

  • Rapamycin decreased cellular hypertrophy and SA-β-Gal staining in MEFs but also inhibited proliferation.
  • Rapamycin showed partial senescence suppression at 30 pM in MEFs, but this was counteracted by cytostatic effects.
  • Rapamycin treatment in REFs allowed cells to overcome replicative senescence, with senescent phenotypes disappearing after treatment cessation.

Conclusions:

  • Rapamycin can partially suppress replicative senescence in rodent cells.
  • Balancing the anti-aging effects of rapamycin with its cytostatic properties is crucial for therapeutic applications.
  • Rapamycin treatment can enable recovery from replicative senescence, suggesting potential for rejuvenation strategies.

More Related Videos

Mouse Round Spermatid Injection08:41

Mouse Round Spermatid Injection

Published on: January 26, 2024

The Replica Set Method: A High-throughput Approach to Quantitatively Measure Caenorhabditis elegans Lifespan11:58

The Replica Set Method: A High-throughput Approach to Quantitatively Measure Caenorhabditis elegans Lifespan

Published on: June 29, 2018

Related Concept Videos

Replicative Cell Senescence02:15

Replicative Cell Senescence

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 the telomeric...
Replicative Cell Senescence02:15

Replicative Cell Senescence

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 the telomeric...
Experimental RNAi02:15

Experimental RNAi

RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...