Hepassocin is required for hepatic outgrowth during zebrafish hepatogenesis
- Gao, M., Yan, H., Yin, R.H., Wang, Q., Zhan, Y.Q., Yu, M., Ge, C.H., Li, C.Y., Wang, X.H., Ge, Z.Q., Yang, X.M.
- Biochemical and Biophysical Research Communications 463(3): 466-71 (Journal)
- Registered Authors
- Wang, Qiang
- HPS, hepatocyte proliferation, liver development, zebrafish
- MeSH Terms
- Cell Proliferation
- Gene Expression Regulation, Developmental
- Gene Knockdown Techniques
- Intercellular Signaling Peptides and Proteins/genetics
- Intercellular Signaling Peptides and Proteins/metabolism*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- 26047702 Full text @ Biochem. Biophys. Res. Commun.
Gao, M., Yan, H., Yin, R.H., Wang, Q., Zhan, Y.Q., Yu, M., Ge, C.H., Li, C.Y., Wang, X.H., Ge, Z.Q., Yang, X.M. (2015) Hepassocin is required for hepatic outgrowth during zebrafish hepatogenesis. Biochemical and Biophysical Research Communications. 463(3):466-71.
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.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes