| First Author | Wu Q | Year | 1998 |
| Journal | J Clin Invest | Volume | 101 |
| Issue | 2 | Pages | 321-6 |
| PubMed ID | 9435303 | Mgi Jnum | J:45393 |
| Mgi Id | MGI:1195365 | Doi | 10.1172/JCI1617 |
| Citation | Wu Q, et al. (1998) Generation and characterization of mice deficient in hepsin, a hepatic transmembrane serine protease. J Clin Invest 101(2):321-6 |
| abstractText | Hepsin is a type II transmembrane serine protease highly expressed on the surface of hepatocytes. The physiological function of hepsin is not known, although in vitro studies indicate that hepsin plays a role in the initiation of blood coagulation and in hepatocyte growth. To determine the functional importance of hepsin, we generated hepsin-deficient mice by homologous recombination. Homozygous hepsin-/- mice were viable and fertile, and grew normally. In functional assays including tail bleeding time, plasma clotting times, and tissue factor- or LPS-induced disseminated intravascular coagulation models, no significant difference was found between hepsin-/- and wild-type litter mates. Liver weight and serum concentrations of liver-derived proteins or enzymes were similar in hepsin-/- and wild-type mice. Interestingly, serum concentrations of bone-derived alkaline phosphatase were approximately twofold higher in hepsin-/- mice of both sexes when compared with wild-type litter mates. No obvious abnormalities were found in major organs in hepsin-/- mice in histological examinations. Our results indicate that hepsin is not essential for embryonic development and normal hemostasis. Hepsin-/- mice will help to evaluate the long-term effects of hepsin deficiency in these animals. |
