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Gene targeting in hemostasis. Hepsin.

¹Cardiovascular Research, Berlex Biosciences, Richmond, CA94804, USA. qingyu_wu@berlex.com

Frontiers in Bioscience : a Journal and Virtual Library

|February 15, 2001

Summary

Hepsin deficiency in mice did not impact hemostasis, liver function, or development. However, hepsin knockout mice unexpectedly showed elevated bone-derived alkaline phosphatase levels, suggesting a potential role in bone metabolism.

Area of Science:

Biochemistry
Genetics
Physiology

Background:

Hepsin is a type II transmembrane serine protease found on hepatocytes.
In vitro studies suggest hepsin's involvement in blood coagulation, hepatocyte growth, and fertilization.

Purpose of the Study:

To investigate the functional significance of hepsin in vivo.
To determine the physiological roles of hepsin using a genetically engineered mouse model.

Main Methods:

Generation of hepsin-deficient (hepsin-/-) mice via homologous recombination.
Comprehensive analysis of hemostasis, liver function, development, and organ histology in hepsin-/- mice compared to wild-type controls.

Main Results:

Hepsin-/- mice were viable, fertile, and exhibited normal growth and development.

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Hemostasis assays, liver function tests, and histological examinations revealed no significant differences between hepsin-/- and wild-type mice.

A notable finding was a two-fold increase in serum bone-derived alkaline phosphatase in hepsin-/- mice of both sexes.

Conclusions:

Hepsin is not essential for normal hemostasis, embryogenesis, or liver function.
Hepsin deficiency leads to elevated serum bone-derived alkaline phosphatase, indicating a potential role in bone metabolism that warrants further investigation.