Hepassocin is required for hepatic outgrowth during zebrafish hepatogenesis

Journal Article · Fri Jul 31 00:00:00 EDT 2015 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/J.BBRC.2015.05.121· OSTI ID:22462129

Gao, Ming ^[1]; Yan, Hui ^[2]; Yin, Rong-Hua ^[3]; Wang, Qiang ^[4]; Zhan, Yi-Qun; Yu, Miao; Ge, Chang-Hui; Li, Chang-Yan; Wang, Xiao-Hui ^[3]; Ge, Zhi-Qiang ^[1]; Yang, Xiao-Ming ^[1]

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1. Tianjin University, Department of Pharmaceutical Engineering, Tianjin 300072 (China)
2. Beijing Institute of Pharmacology and Toxicology, Beijing 100850 (China)
3. Beijing Institute of Radiation Medicine, Beijing 100850 (China)
4. Institute of Zoology, Chinese Academy of Sciences, Beijing 100101 (China)

Background & aims: Hepassocin (HPS) is a hepatotrophic growth factor that specifically stimulates hepatocyte proliferation and promotes liver regeneration after liver damage. In this paper, zebrafish were used to investigate the role of HPS in liver development. Methods and results: During zebrafish development, HPS expression is enriched in liver throughout hepatogenesis. Knockdown of HPS using its specific morpholino leads to a smaller liver phenotype. Further results showed that the HPS knockdown has no effect on the expression of the early endoderm marker gata6 and early hepatic marker hhex. In addition, results showed that the smaller-liver phenotype in HPS morphants was caused by suppression of cell proliferation, not induction of cell apoptosis. Conclusions: Current findings indicated that HPS is essential to the later stages of development in vertebrate liver organogenesis. - Highlights: • HPS is enriched in zebrafish liver and has strong similarities with other species. • Knocking down HPS with MOs results in small liver phenotype. • HPS depletion regulates liver outgrowth but not liver specification and budding. • HPS depletion causes hepatocyte proliferation arrest but not apoptosis induction.

• OSTI ID: 22462129
• Journal Information: Biochemical and Biophysical Research Communications, Vol. 463, Issue 3; Other Information: Copyright (c) 2015 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
APOPTOSIS
CARBOXYLIC ACIDS
CELL PROLIFERATION
DAMAGE
FIBRINOGEN
GROWTH FACTORS
HEPATOMAS
INHIBITION
LIVER
PHENOTYPE
SILICON OXIDES
SPECIFICATIONS
VERTEBRATES