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Published on: June 2, 2017

Formation of extracellular matrix-digesting invadopodia by primary aortic smooth muscle cells

Emilia Furmaniak-Kazmierczak1, Scott W Crawley, Rhonda L Carter

  • 1Department of Biochemistry, Queen's University, Kingston, ON, Canada.

Circulation Research
|April 21, 2007
PubMed

Insights

Vascular smooth muscle cells (VSMCs) can form invadopodia-like structures, similar to those in cancer cells, which degrade extracellular matrix. This process is regulated by specific signaling pathways and proteins, potentially contributing to cardiovascular disease.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Cardiovascular Research

Background:

  • Vascular smooth muscle cell (VSMC) invasion of the subendothelial space is implicated in cardiovascular diseases.
  • Understanding VSMC behavior is crucial for developing therapeutic strategies.

Purpose of the Study:

  • To investigate the mechanisms by which VSMCs form extracellular matrix-degrading structures.
  • To identify key signaling molecules and pathways involved in VSMC invasion.

Main Methods:

  • Primary rat aorta VSMCs were induced to form invadopodia-like structures.
  • Expression of activated Src, Cdc42, Rac1, and kinase-dead PAK1 was analyzed.
  • Matrix degradation and invadopodia marker expression (cortactin, MMP-9, MT1-MMP, uPAR) were assessed.
  • Signaling pathway involvement (ERK, p38 MAPK) was investigated.

Main Results:

  • Activated Src, Cdc42, Rac1, or kinase-dead PAK1 induced VSMCs to form actin-rich, matrix-degrading protrusions resembling invadopodia.
  • These structures contained invadopodia markers and matrix metalloproteinases (MMP-9, MT1-MMP) and uPAR.
  • Invadopodia formation by Src depended on Cdc42, Rac, and ERK, but not p38 MAPK.
  • Kinase-dead PAK1-induced invadopodia required Src and ERK activity and PIX interaction.
  • VSMCs in 3D collagen matrices formed matrix-penetrating extensions.

Conclusions:

  • VSMCs can form invadopodia-like structures capable of extracellular matrix degradation.
  • Src, Cdc42, Rac1, PAK1, ERK, and PIX are key regulators of this process.
  • These findings offer insights into VSMC behavior in cardiovascular disease pathogenesis.

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