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A Novel Murine Model of Arteriovenous Fistula Failure: The Surgical Procedure in Detail

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The mouse arteriovenous fistula model.

Binxia Yang¹, Uday Shergill, Alex A Fu

¹Department of Radiology, Mayo Clinic College of Medicine, 200 First Street Southwest, Alfred 6460, Rochester, MN 55905, USA.

Journal of Vascular and Interventional Radiology : JVIR

|June 27, 2009

Summary

A new mouse model of arteriovenous (AV) fistula was developed. This model showed increased expression of matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 in venous stenosis.

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Area of Science:

Vascular biology
Surgical modeling
Biomarker analysis

Background:

Arteriovenous (AV) fistula creation is crucial for hemodialysis access.
Venous stenosis is a common complication of AV fistulas, leading to access failure.
Understanding the molecular mechanisms underlying AV fistula stenosis is essential for developing effective treatments.

Purpose of the Study:

To establish a mouse model of carotid artery-to-jugular vein arteriovenous (AV) fistula.
To investigate the gene expression of matrix metalloproteinase (MMP)-2 and MMP-9 in the venous stenosis of the AV fistula model.

Main Methods:

An AV fistula was surgically created in FVB/NJ mice, with contralateral vessels serving as controls.
Reverse transcriptase polymerase chain reaction and immunohistochemical analysis were used to assess gene and protein expression.

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Key markers including MMP-2, MMP-9, TIMP-1, and TIMP-2 were quantified at the venous stenosis site.

Main Results:

Venous stenosis developed at the outflow vein, characterized by neointimal thickening.
Significantly increased expression of MMP-2, TIMP-1, and TIMP-2 was observed at the venous stenosis by day 28 compared to controls.
Alpha-smooth muscle actin staining confirmed cellular changes in the neointima.

Conclusions:

A reproducible mouse model for studying AV fistula venous stenosis was successfully developed.
The model demonstrated elevated expression of MMP-2, TIMP-1, and TIMP-2, suggesting their involvement in AV fistula stenosis pathogenesis.
This model provides a valuable tool for future research into the mechanisms driving AV fistula venous stenoses.