Related Experiment Video

Updated: Jul 6, 2026

Induction and Validation of Cellular Senescence in Primary Human Cells
08:18

Induction and Validation of Cellular Senescence in Primary Human Cells

Published on: June 20, 2018

Nuclear swelling occurs during premature senescence mediated by MAP kinases in normal human fibroblasts

Yusuke Kobayashi1, Risa Sakemura, Atsuko Kumagai

  • 1Kihara Institute for Biological Research, Graduate School of Integrated Science, Yokohama City University, 641-12 Maioka-cho, Yokohama 244-0813, Japan.

Bioscience, Biotechnology, and Biochemistry
|April 9, 2008
PubMed

Insights

Excess thymidine causes premature cell aging in human fibroblasts, triggering senescence markers and cell swelling. Mitogen-activated protein (MAP) kinase inhibitors blocked this aging process, suggesting a role for MAP kinase signaling in thymidine-induced senescence.

Area of Science:

  • Cellular senescence research
  • Molecular biology of aging
  • Fibroblast cell culture models

Background:

  • Cellular senescence is a state of irreversible growth arrest.
  • Thymidine, a DNA precursor, can influence cellular processes.
  • Mitogen-activated protein (MAP) kinases are key signaling pathways involved in cellular responses.

Purpose of the Study:

  • To investigate the effect of excess thymidine on normal human fibroblasts.
  • To identify the role of MAP kinase signaling in thymidine-induced premature senescence.

Main Methods:

  • Treatment of TIG-7 human fibroblasts with excess thymidine.
  • Observation of cellular morphology and senescence markers.
  • Application of specific MAP kinase inhibitors (U0126, SB203580, SP60025).

Main Results:

  • Excess thymidine induced premature senescence in fibroblasts.
  • Senescent cells exhibited nuclear and cell swelling.
  • MAP kinase inhibitors significantly suppressed thymidine-induced senescence and its markers.

Conclusions:

  • Excess thymidine can trigger premature senescence in human fibroblasts.
  • MAP kinase signaling pathways are involved in the mechanism of thymidine-induced senescence.
  • Inhibiting MAP kinases offers a potential strategy to mitigate thymidine-induced cellular aging.

More Related Videos

Detection of Nuclear Blebbing and DNA Leakage in Mammalian Cells by Immunofluorescence06:23

Detection of Nuclear Blebbing and DNA Leakage in Mammalian Cells by Immunofluorescence

Published on: January 17, 2025

Techniques to Induce and Quantify Cellular Senescence06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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...
Cells Coordinate Growth and Proliferation02:36

Cells Coordinate Growth and Proliferation

Cell size is a significant factor impacting cellular design, function, and fitness. There exists some internal coordination by which cells double their masses before division, thus, achieving homeostasis. Coordination between cell growth and proliferation depends on the checkpoints in between cell cycle phases. Loss of coordination or failure in the checkpoint mechanism can drive the cell to uncontrolled growth and loss of cellular function. Like dividing cells that coordinate cellular growth,...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
Disassembly of Intermediate Filaments01:35

Disassembly of Intermediate Filaments

Intermediate filaments (IFs) do not undergo spontaneous disassembly. Enzymes, kinases, and phosphatases add and remove phosphates from specific sites to regulate their disassembly. The IF concentration in the cytoplasm also regulates the disassembly. If the concentration crosses a threshold, it activates the protein kinases in the vicinity, allowing the phosphorylation of IFs.
Keratin proteins, found at the cell periphery near cell junctions, undergo a cycle of assembly and disassembly. In Type...