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Neonatal growth delay in alpha-1-antitrypsin disease. Influence of genetic background

M J Dycaico1, K Felts, S W Nichols

  • 1Stratagene, La Jolla, CA 92037.

Molecular Biology & Medicine
|April 1, 1989
PubMed

Insights

A new transgenic mouse model, Z#2, mimics alpha 1-protease inhibitor (alpha 1-Pi)-associated liver disease in humans. This model exhibits non-viral hepatitis and growth retardation, offering insights into disease variability.

Area of Science:

  • Hepatology
  • Genetics
  • Animal Models

Background:

  • Alpha 1-protease inhibitor (alpha 1-Pi) deficiency causes liver disease in humans.
  • A subset of affected infants develop non-viral hepatitis and growth retardation.
  • Genetic factors influence disease severity in human families.

Purpose of the Study:

  • To develop a mouse model for alpha 1-Pi-associated liver disease.
  • To investigate the genetic basis of phenotypic variability in alpha 1-Pi liver disease.

Main Methods:

  • Development of a Z#2 transgenic mouse strain.
  • Crossbreeding Z#2 mice with DBA/2J and CBA/J inbred mouse strains.
  • Phenotypic analysis of transgenic offspring for hepatitis and growth retardation.

Main Results:

  • The Z#2 mouse strain spontaneously develops non-viral hepatitis and growth retardation.
  • Phenotypic severity varied based on the genetic background of the crossed inbred mice.
  • Crosses with DBA/2J mice showed more pronounced phenotypes compared to CBA/J mice.

Conclusions:

  • The Z#2 mouse is a viable model for alpha 1-Pi-associated liver disease.
  • Genetic background significantly influences the manifestation of alpha 1-Pi liver disease.
  • This model can be used to study disease mechanisms and potential therapeutic strategies.

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