mir122 deficiency inhibits differentiation of zebrafish hepatoblast into hepatocyte
- Authors
- Xu, R.R., Zhang, C.W., Cao, Y., and Wang, Q.
- ID
- ZDB-PUB-130610-28
- Date
- 2013
- Source
- Yi chuan = Hereditas 35(4): 488-494 (Journal)
- Registered Authors
- Wang, Qiang
- Keywords
- none
- MeSH Terms
-
- Animals
- Cell Differentiation/genetics*
- Embryo, Nonmammalian/cytology*
- Embryo, Nonmammalian/metabolism
- Hepatocytes/cytology*
- MicroRNAs/genetics*
- MicroRNAs/metabolism*
- Zebrafish/embryology*
- Zebrafish/genetics*
- PubMed
- 23659939 Full text @ Yi Chuan
As one of the largest internal organs in the body, liver is very important for metabolism, detoxification and homeostasis. It's reported that liver development is accurately regulated by a gene regulating network consists of FGF, BMP, WNT signal pathways and a lot of transcription factors. However, the functions of microRNA are poorly understood during liver formation. In recent years, it has been reported that mir122 is highly expressed in hepatocytes, and plays a vital role in the metabolic processes of the liver, but its function in liver development remains unclear. In this study, we report that mir122 is specifically expressed in zebrafish (Danio rerio) embryonic liver, and its expression level is notably increased during the differentiation process of hepatoblast into hepatocyte. mir122 inactivation by an antisense morpholino has no influence on the specification, budding and outgrowth of hepatoblast. However, zbrafish hepatoblast can not differentiate into hepatocyte without mir122. Therefore, mir122 is not only involved in liver metabolic functions, but also indispensable for hepatoblast differentiation.