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Collateral density, remodeling, and VEGF-A expression differ widely between mouse strains.

Dan Chalothorn1, Jason A Clayton, Hua Zhang

  • 1Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill, North Carolina 27599-7545, USA.

Physiological Genomics
|April 12, 2007
PubMed
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BALB/c mice have fewer pre-existing blood collaterals and impaired collateral growth compared to C57BL/6 mice, potentially due to lower VEGF-A expression. This genetic difference offers a model for studying collateral formation in ischemia.

Area of Science:

  • Cardiovascular Biology
  • Genetics
  • Ischemia Research

Background:

  • Significant inter-species variability exists in collateral vessel density and ischemia-induced collateral growth.
  • The underlying genetic mechanisms governing collateral formation and remodeling remain largely unknown.

Purpose of the Study:

  • To investigate the mechanisms behind differences in collateral density and ischemia-induced collateral growth between two mouse strains, BALB/c and C57BL/6.
  • To identify potential genetic factors contributing to these observed variations.

Main Methods:

  • Femoral artery ligation was performed in BALB/c and C57BL/6 mice to assess hindlimb perfusion and collateralization.
  • Angiography, immunohistochemistry, and gene expression analysis (VEGF-A) were employed.
  • Recombinant inbred strains were analyzed to identify quantitative trait loci associated with VEGF-A mRNA abundance.

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Main Results:

  • BALB/c mice exhibited significantly lower baseline collateral density and impaired hindlimb perfusion recovery post-ligation compared to C57BL/6 mice.
  • BALB/c mice showed reduced collateral remodeling, angiogenesis, and impaired hindlimb use, associated with lower TNF-alpha expression.
  • Reduced collateralization was also observed in other tissues of BALB/c mice, including intestine and pial circulation, with attenuated ischemic induction of VEGF-A.
  • A quantitative trait locus for VEGF-A mRNA abundance was identified near the Vegfa locus, associating with lower expression in BALB/c mice, suggesting a cis-acting polymorphism.

Conclusions:

  • BALB/c and C57BL/6 mouse strains display marked differences in collateral vessel formation and response to ischemia.
  • Reduced VEGF-A expression, potentially due to a Vegfa gene polymorphism, may underlie the deficiencies in collateral growth observed in BALB/c mice.
  • These mouse strains provide a valuable model for exploring the genetic determinants of collateral development and therapeutic strategies for ischemic diseases.