J. Lipid Res.
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A more recent version of this article appeared on October 1, 2005

Papers In Press, published online ahead of print July 16, 2005
J. Lipid Res., doi:10.1194/jlr.M500179-JLR200
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Submitted on May 9, 2005
Revised on July 5, 2005
Accepted on July 10, 2005

Plasma HDL in human apoA-I transgenic-Abca1 knockout mice undergo normal intravascular remodeling but are hypercatabolized by the kidney

Ji-Young Lee, Jenelle M. Timmins, Anny Mulya, Thomas L. Smith, Yiwen Zhu, Edward M. Rubin, Jeffrey W. Chisholm, Perry L. Colvin, and John S. Parks

Pathology Dept., Wake Forest University School of Medicine, Winston-Salem, NC 27157

Corresponding Author: jparks{at}wfubmc.edu

Patients homozygous for Tangier disease have a near absence of plasma HDL due to mutations in ABCA1 and hypercatabolize normal HDL particles. To determine the relationship between ABCA1 expression and HDL catabolism, we investigated intravascular remodeling, plasma clearance, and organ-specific uptake of HDL in mice expressing the human apoA-I transgene (hA-I Tg) in the Abca1-/- knockout (KO) background. Small HDL particles (7.5 nm), radiolabeled with 125I-tyramine cellobiose, were injected into recipient mice to quantify plasma turnover and organ uptake of tracer. Small HDL tracer was remodeled to 8.2 nm diameter particles within 5 min in hA-I Tg mice (control) and KO mice. Decay of tracer from plasma was 1.6-fold more rapid in KO mice (p<0.05) and kidney uptake was twice that of controls, with no difference in liver uptake. We also observed a two-fold higher hepatic expression of ABCA1 protein in hA-I Tg mice, compared to non-transgenic mice, suggesting that overexpression of human apoA-I sta-bilized hepatic ABCA1 protein in vivo. We conclude that ABCA1 is not required for in vivo remodeling of small HDL to larger HDL subfractions and that hypercatabolism of normal HDL particles in KO mice is due to a selective catabolism of HDL apoA-I by the kidney.


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