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In animal cells, the extracellular matrix allows cells within tissues to withstand external stresses and transmits signals from the outside of the cell to the inside. The extracellular matrix is extensive, and its composition varies between different types of tissues. For example, the reticular fibers and ground substance make up the ECM in loose connective tissue, while collagen and bone minerals make up the ECM of bone tissue. 
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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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Updated: Mar 28, 2026

Engineering Fibrin-based Tissue Constructs from Myofibroblasts and Application of Constraints and Strain to Induce Cell and Collagen Reorganization
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Myofibroblast persistence with real-time changes in boundary stiffness.

Mehmet H Kural1, Kristen L Billiar1

  • 1Department of Biomedical Engineering, Worcester Polytechnic Institute, Worcester, MA, USA.

Acta Biomaterialia
|December 30, 2015
PubMed
Summary

Mechanical forces influence myofibroblast behavior. Reducing tension can trigger apoptosis or dedifferentiation, offering therapeutic potential for fibrotic diseases and tissue engineering.

Keywords:
ApoptosisFibrinMechanobiologyMyofibroblastStiffnessTGF-β1TensionThree-dimensionalValvular interstitial cell

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Area of Science:

  • Cell biology
  • Biomedical engineering
  • Tissue mechanics

Background:

  • Myofibroblasts are crucial for wound healing and tissue remodeling.
  • Excessive myofibroblast activity contributes to fibrotic diseases and tissue thickening.
  • The mechanisms of myofibroblast clearance (dedifferentiation vs. apoptosis) are debated.

Purpose of the Study:

  • To investigate the hypothesis that mechanical inhibition of myofibroblast force generation induces de-differentiation or apoptosis.
  • To determine the effect of varying degrees of tension reduction on myofibroblast fate.
  • To explore therapeutic strategies for controlling myofibroblast populations in engineered tissues.

Main Methods:

  • Valvular interstitial cells (VICs) were cultured in fibrin micro-tissues suspended between flexible posts.
  • Magnetic forces were applied to modulate post stiffness and thus cellular tension in real-time.
  • Cellular tension, α-SMA expression, and apoptosis rates were measured under different mechanical conditions.

Main Results:

  • Increased boundary stiffness elevated cell-generated forces.
  • Temporary stiffening led to sustained force generation even after stiffness reduction.
  • Complete release from posts induced apoptosis and reduced α-SMA staining.
  • A significant reduction in tension was required to trigger dedifferentiation and/or apoptosis.

Conclusions:

  • Temporary increases in myofibroblast force generation can have lasting effects on their persistence.
  • The magnitude of tension reduction dictates whether myofibroblasts undergo dedifferentiation or apoptosis.
  • Controlling mechanical tension offers a promising approach for therapeutic interventions and tissue engineering.