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Introduction to Fibroblasts01:09

Introduction to Fibroblasts

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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Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
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Published on: June 14, 2016

S100A4 Orchestrates Fibroblast Fate to Drive Fibrotic Remodeling.

Spring Li1, Banruo Cai1, Xu Zhang1

  • 1Division of Molecular and Translational Biomedicine, Department of Anesthesiology & Perioperative Medicine, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|June 13, 2026
PubMed
Summary

S100A4 protein promotes fibroblast survival and activation, driving fibrotic lung diseases like idiopathic pulmonary fibrosis (IPF). Blocking the ERK signaling pathway it engages may offer new therapeutic strategies for fibrosis.

Keywords:
ERK signalingS100A4extracellular matrix remodelingfibroblast activationfibroblast fatefibroblast survivalidiopathic pulmonary fibrosispulmonary fibrosis

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09:50

Fibroblast Derived Human Engineered Connective Tissue for Screening Applications

Published on: August 20, 2021

Area of Science:

  • Cell Biology
  • Pulmonary Medicine
  • Molecular Biology

Background:

  • Fibrotic diseases, including idiopathic pulmonary fibrosis (IPF), are driven by persistent, activated fibroblasts.
  • Fibroblasts normally undergo apoptosis after wound repair but evade this in fibrotic conditions.
  • The precise mechanisms by which S100A4 protein contributes to fibroblast persistence and activation in fibrosis are not fully understood.

Purpose of the Study:

  • To elucidate the role of S100A4 in regulating fibroblast survival and activation in fibrotic lung disease.
  • To investigate the involvement of extracellular signal-regulated kinase (ERK) signaling in S100A4-mediated fibroblast functions.
  • To assess the therapeutic potential of targeting S100A4 and ERK in pulmonary fibrosis.

Main Methods:

  • Primary murine lung fibroblasts were treated with S100A4 to assess activation and apoptosis resistance.
  • ERK signaling pathway was pharmacologically inhibited to evaluate its role in S100A4 effects.
  • Bleomycin-induced lung injury model in mice was used to study fibrotic remodeling and S100A4 expression.
  • Primary lung fibroblasts from IPF patients were analyzed for S100A4 and ERK pathway activation.
  • siRNA-mediated knockdown of S100A4 was performed in IPF fibroblasts.

Main Results:

  • S100A4 activates ERK signaling in fibroblasts, promoting migration, ECM contractility, and alpha-smooth muscle actin (α-SMA) expression.
  • S100A4 confers resistance to apoptosis induced by pro-apoptotic and oxidative stress stimuli.
  • ERK inhibition attenuates S100A4-driven fibroblast activation and survival.
  • Bleomycin-induced lung injury shows increased S100A4 expression and fibrotic remodeling.
  • IPF fibroblasts exhibit elevated S100A4, enhanced ERK activation, and increased α-SMA.
  • S100A4 knockdown in IPF fibroblasts reduces ERK activation and profibrotic gene expression.

Conclusions:

  • S100A4 is a key regulator of apoptosis-resistant, profibrotically activated fibroblasts via ERK signaling.
  • This S100A4-ERK axis contributes to pathological matrix remodeling in pulmonary fibrosis.
  • S100A4 and ERK signaling represent potential therapeutic targets for treating pulmonary fibrosis.