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Updated: Aug 12, 2026
Mouse Kidney Transplantation: Models of Allograft Rejection
Published on: October 11, 2014
Deficiency of a kidney metalloproteinase activity in inbred mouse strains
Abstract:
Kidneys from BALB/c mice contain a potent metalloendoproteinase, termed meprin, that is active against large proteins as well as small peptides. The enzyme is present in mouse strains C57BR/cdJ, C57BL/6J, BALB/cJ, A/J, DBA/IJ, CD/l, Swiss, and ICR. Three related inbred strains, CBA/J, CBA/CaJ, and C3H/He, are markedly deficient in this enzymatic activity. This is the first report of a heritable deficiency of an intracellular proteinase in mammalian tissues. Meprin deficiency appears to have arisen as an early event in the development of the C stock. Furthermore, meprin is present in the progeny of a cross between a meprin-sufficient female (C57BL/6) and a meprin-deficient male (C3H/HeN), an indication that the trait for the deficiency is recessive.
Insights
Mice kidneys possess a potent enzyme called meprin, active against proteins and peptides. A heritable deficiency in meprin was discovered in specific mouse strains, indicating a recessive genetic trait.
Area of Science:
- Biochemistry
- Genetics
- Mammalian Physiology
Background:
- Mice kidneys contain a potent metalloendoproteinase, meprin.
- Meprin exhibits activity against both large proteins and small peptides.
- This enzyme's presence varies across different mouse strains.
Purpose of the Study:
- To investigate the presence and activity of meprin in various mouse strains.
- To identify and characterize strains with a deficiency in meprin enzymatic activity.
- To determine the heritability and inheritance pattern of meprin deficiency.
Main Methods:
- Enzyme assays to measure meprin activity in kidney extracts.
- Comparative analysis of meprin levels across multiple inbred mouse strains.
- Cross-breeding experiments between meprin-sufficient and deficient strains.
Main Results:
- Meprin was found to be present in several mouse strains, including BALB/c, C57BR/cdJ, C57BL/6J, BALB/cJ, A/J, DBA/IJ, CD/l, Swiss, and ICR.
- Three related inbred strains (CBA/J, CBA/CaJ, and C3H/He) showed a marked deficiency in meprin activity.
- Progeny from a cross between a meprin-sufficient and a deficient mouse strain inherited meprin, indicating a recessive deficiency trait.
Conclusions:
- This study reports the first instance of a heritable deficiency of an intracellular proteinase in mammalian tissues.
- Meprin deficiency likely originated early in the development of the C stock.
- The recessive nature of meprin deficiency was confirmed through genetic crosses.
