Thromb Haemost 2000; 84(05): 865-870
DOI: 10.1055/s-0037-1614129
Review Article
Schattauer GmbH

Mice Deficient in Hepsin, a Serine Protease, Exhibit Normal Embryogenesis and Unchanged Hepatocyte Regeneration Ability

I.-Shing Yu
1   From the Graduate Institute of Medical Technology, College of Medicine, National Taiwan University, Taiwan
,
Huei-Jane Chen
2   National Health Research Institute, National Taiwan University Hospital, Taiwan
,
Ying-Shuan E. Lee
2   National Health Research Institute, National Taiwan University Hospital, Taiwan
,
Pei-Hsing Huang
3   Department of Pathology, College of Medicine, National Taiwan University, Taiwan
,
Shu-Rung Lin
4   Institute of Molecular Medicine, College of Medicine, National Taiwan University, Taiwan
,
Tzan-Wu Tsai
5   Laboratory of Animal Center, College of Medicine, National Taiwan University, Taiwan
,
Shu-Wha Lin
1   From the Graduate Institute of Medical Technology, College of Medicine, National Taiwan University, Taiwan
6   Laboratory of Medicine, National Taiwan University Hospital, Taiwan
› Institutsangaben

The authors thank Dr. Li-Tzu Li, Ms Chin-Chin Huang, and Mr. Hsiang-Ming Wang for helpful discussions and technical assistance. Many thanks to Ms Su-Jen Hsu and the clinical chemistry laboratory at the NTUH for providing assistance to blood chemistry analyses. This work is supported by grants to Dr. S. W. Lin from the National Science Counsel (no. NSC89-2318-B002-006-M51), the National Health Research Institute (no.DOH88-HR-811 and NHRIGT-EX89) and The Istitute of Biomedical Sciences, Academia Sinica, Taiwan (no. IBMS-CRC86-T06, -CRC87-T05, and -CRC88-T09).
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Publikationsverlauf

Received 01. Mai 2000

Accepted after revision 31. Mai 2000

Publikationsdatum:
13. Dezember 2017 (online)

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Summary

Hepsin, a liver-enriched novel serine protease, has been implicated in participating with normal cell growth, embryogenesis, and blood coagulation pathway. To study its function in vivo, we have disrupted the mouse hepsin gene by homologous recombination. Targeted disruption of the hepsin gene and ablation of hepsin message were demonstrated by Southern blotting, Northern blotting and RT-PCR analysis. Homozygous hepsin −/− mice were viable, fertile, and exhibited no gross abnormalities, as judged by the size, weight and blood coagulation (PT) assays. However, the serum concentration of the bone form of alkaline phosphatase, aspartate aminotransferase, and alanine aminotransferase of the hepsin −/− mice was mildly elevated, in spite of no obvious pathological change of hepatocytes. To examine whether hepsin is involved in controlling cell growth in adult tissues, 70% hepatectomy was applied to the hepsin −/− mice. Liver regeneration proceeded normally in the hepsin −/− mice as judged by the liver mass restoration rate. These results suggest that loss of hepsin function causes no effect in cell growth and embryogenesis in vivo, which is in contradiction to the studies using in vitro cell culturing system. Moreover, gross mass regeneration of liver after damage proceeds normally in the absence of functional hepsin.