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Regulation of corneal fibroblast MMP-1 secretion by cytochalasins

M B Berman1

  • 1Department of Ophthalmology, University of Texas Southwestern Medical Center at Dallas.

Cornea
|January 1, 1994
PubMed

Insights

Cytochalasins disrupt fibroblast F-actin, causing fibronectin loss and increasing latent collagenase (MMP-1). This suggests intracellular disruption of microfilaments can modulate extracellular matrix remodeling via fibronectin receptors.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Extracellular Matrix Research

Background:

  • Fibronectin (Fn) and F-actin microfilaments are crucial for cell adhesion and tissue structure.
  • Type I interstitial collagenase (MMP-1) plays a role in extracellular matrix degradation.
  • Integrin receptors mediate cell-matrix interactions.

Purpose of the Study:

  • To investigate the effects of cytochalasins B, dihydroB, and D on corneal fibroblasts.
  • To compare the cellular responses to cytochalasins with those induced by plasmin.
  • To elucidate the mechanisms by which cytochalasins modulate collagenase secretion.

Main Methods:

  • Treatment of normal rabbit corneal fibroblasts with cytochalasins (CB, H2CB, CD).
  • Analysis of fibronectin localization on the cell surface.
  • Assessment of F-actin microfilament bundle integrity.
  • Quantification of type I interstitial collagenase (MMP-1) in the culture medium.

Main Results:

  • Cytochalasins caused loss of cell-surface fibronectin and breakdown of F-actin stress fibers.
  • Increased levels of latent MMP-1 were observed in the medium after cytochalasin treatment.
  • Cytochalasins induced withdrawal from the fibronectin mesh without complete loss, unlike plasmin.
  • Results suggest cytochalasins perturb the alpha 5 beta 1 integrin (Fn) receptor via intracellular F-actin disruption.

Conclusions:

  • Both extracellular plasmin and intracellular cytochalasins can modulate MMP-1 secretion by corneal fibroblasts through fibronectin receptor perturbation.
  • Cytochalasins disrupt F-actin, leading to altered Fn receptor function and fibronectin loss.
  • Secretion and activation of collagenase can be uncoupled, as evidenced by the latent form after cytochalasin treatment.

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