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

Journal: Thrombosis and Haemostasis
ISSN: 0340-6245
Issue: 2000: 84/5 (Nov) pp.740-934
Pages: 865-870

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

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

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.