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Rudolph Virchow discovered spindle-shaped cells called fibroblasts in 1858. Inactive fibroblasts, called fibrocytes, become activated by various stimuli, such as growth factors and inflammatory cytokines. Activated fibroblasts play a crucial role in wound healing, inflammation, formation of new blood vessels, and cancer progression. Uncontrolled activation of fibroblasts results in fibrosis, the excess deposition of fibrous tissue, which can lead to scarring and affect normal organs. This...
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A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth
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Published on: December 22, 2020

Normal or stress-induced fibroblast senescence involves COX-2 activity.

Stéphanie Zdanov1, David Bernard, Florence Debacq-Chainiaux

  • 1Research Unit on Cellular Biology (URBC), University of Namur (FUNDP), rue de Bruxelles, 61 B-5000 Namur, Belgium.

Experimental Cell Research
|June 15, 2007
PubMed
Summary

Cyclooxygenase-2 (COX-2) drives fibroblast senescence. Inhibiting COX-2 delays senescence markers, indicating its crucial role in aging and stress responses.

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Techniques to Induce and Quantify Cellular Senescence
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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

Area of Science:

  • Cell Biology
  • Biochemistry
  • Aging Research

Background:

  • Cyclooxygenase-2 (COX-2) is an inducible enzyme in prostaglandin synthesis.
  • COX-2 activity can cause oxidative damage and is implicated in cellular stress responses.

Purpose of the Study:

  • To investigate the role of COX-2 in fibroblast senescence.
  • To determine if COX-2 activity contributes to the development of senescent characteristics.

Main Methods:

  • Assessed COX-2 expression and prostaglandin E(2) (PGE(2)) production in senescent human fibroblasts.
  • Manipulated COX-2 activity using arachidonic acid and the inhibitor NS398.
  • Examined senescence markers including cell size, SA-beta-Gal activity, and growth arrest.
  • Investigated COX-2 in NF-kappaB- or H(2)O(2)-induced senescence models.

Main Results:

  • COX-2 expression and PGE(2) production increased ~10-fold during normal fibroblast senescence.
  • Enhanced COX-2 activity accelerated senescence markers; inhibition partially prevented them.
  • COX-2 and PGE(2) also increased ~10-fold in NF-kappaB- or H(2)O(2)-induced senescence.
  • NS398 or COX-2 siRNA attenuated SA-beta-Gal activity and growth arrest in stress-induced senescence.

Conclusions:

  • COX-2 is significantly upregulated in both normal and stress-induced fibroblast senescence.
  • COX-2 activity is a key contributor to the establishment of senescent cell characteristics.