ZFIN ID: ZDB-PUB-150607-3
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.
Date: 2015
Source: Biochemical and Biophysical Research Communications   463(3): 466-71 (Journal)
Registered Authors: Wang, Qiang
Keywords: HPS, hepatocyte proliferation, liver development, zebrafish
MeSH Terms:
  • Animals
  • Cell Proliferation
  • Gene Expression Regulation, Developmental
  • Gene Knockdown Techniques
  • Hepatocytes/cytology
  • Hepatocytes/metabolism
  • Intercellular Signaling Peptides and Proteins/genetics
  • Intercellular Signaling Peptides and Proteins/metabolism*
  • Liver/embryology*
  • Liver/metabolism
  • Morpholinos/genetics
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed: 26047702 Full text @ Biochem. Biophys. Res. Commun.
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ABSTRACT
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.
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.
Current findings indicated that HPS is essential to the later stages of development in vertebrate liver organogenesis.
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