Transgenic Rabbits: A Novel Model for the Study of Atherosclerosis

@inproceedings{Fan2002TransgenicRA,
  title={Transgenic Rabbits: A Novel Model for the Study of Atherosclerosis},
  author={Jianglin Fan and Masahiro Araki and Lihua Wu and Mireille Challah and Hiroaki Shimoyamada and Richard M. Lawn and Hirotoshi Kakuta and Hisataka Shikama and Teruo Watanabe},
  year={2002}
}
JIANGLIN FAN*, MASAHIRO ARAKI*, LIHUA WU*, MIREILLE CHALLAH*, HIROAKI SHIMOY AMADA*, RICHARD M. LAWN†, HIROTOSHI KAKUTA§, HISATAKA SHIKAMA§ AND TERUO WATANABE*. *Department of Pathology, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba 305-8575, Japan †Falk Cardiovascular Research Center, Stanford University, Stanford, California 94305 §Tsukuba Research Center ofYamanouchi Pharmaceutical Company, Tsukuba, 305, Japan 

References

SHOWING 1-10 OF 11 REFERENCES

Transgenic rabbit models for the study of atherosclerosis.

  • J. TaylorJ. Fan
  • Biology
    Frontiers in bioscience : a journal and virtual library
  • 1997
Recently established lines of transgenic rabbits that overexpress hepatic lipase and apolipoprotein E are yielding fresh insights into the functions of these proteins and their role in lesion development.

Hereditary Hyperlipidemia and Atherosclerosis in the Rabbit Due to Overproduction of Lipoproteins: II. Preliminary Report of Arterial Pathology

A genetically determined hyperlipidemic strain of New Zealand White rabbit that has features in common with combined familialhyperlipidemia in humans has been identified and is a useful new model for the study of atherogenesis.

In vivo model systems: the choice of the experimental animal model for analysis of lipoproteins and atherosclerosis

Emphasis is currently being placed not only on the development of mutant strains of several species that express specific phenotypes, but also on thedevelopment of transgenic models to test suspected gene action on lipoprotein synthesis and metabolism, and vascular pathophysiology.

Serial inbreeding of rabbits with hereditary hyperlipidemia (WHHL-rabbit).

Transgenic mouse models of lipoprotein metabolism and atherosclerosis.

  • J. Breslow
  • Biology
    Proceedings of the National Academy of Sciences of the United States of America
  • 1993
Lipoprotein transport genes have either been added to the germ line of mice by transgenic techniques or knocked out by homologous recombination in embryonic stem cells, resulting in new insights about how they function in the body and their role in lipoprotein metabolism.

Overexpression of human apolipoprotein B-100 in transgenic rabbits results in increased levels of LDL and decreased levels of HDL.

Prior findings in mice, together with the present findings in transgenic rabbits, suggest that triglyceride-rich LDL and lowered levels of HDL cholesterol may be hallmark features of apoB overexpression.

Hereditary Hyperlipidemia in the Rabbit Due to Overproduction of Lipoproteins: I. Biochemical Studies

The hyperlipidemia in this strain of rabbits may be unique in that the underlying mechanism appears to be overproduction of VLDL and LDL, which had increased free cholesterol and esterified cholesterol content, and triglyceride content was reduced.

Overexpression of hepatic lipase in transgenic rabbits leads to a marked reduction of plasma high density lipoproteins and intermediate density lipoproteins.

  • J. FanJ. Wang J. Taylor
  • Biology, Medicine
    Proceedings of the National Academy of Sciences of the United States of America
  • 1994
It is demonstrated that HL functions in the metabolism of HDL and IDL, thereby playing a key role in plasma cholesterol homeostasis.

Apolipoprotein B mRNA-editing protein induces hepatocellular carcinoma and dysplasia in transgenic animals.

The findings compromise the potential use of APOBEC-1 for gene therapy to lower plasma levels of low density lipoproteins and suggests that aberrant editing of hepatic mRNAs involved in cell growth and regulation is the cause of the tumorigenesis.

Increased expression of apolipoprotein E in transgenic rabbits results in reduced levels of very low density lipoproteins and an accumulation of low density lipoproteins in plasma.

It is suggested that the increased content of apo E3 on triglyceride-rich remnant lipoproteins in transgenic rabbits confers a greater affinity for cell surface receptors, thereby increasing remnant clearance from plasma.