Liver has a high level of Alpha-fetoprotein which is assumed to be important for mammalian development. However, Alpha-fetoprotein knockout studies in mice suggested that despite the absence of Alpha-fetoprotein, mice developed normally; the only abnormality observed was infertility in female mice. There are indications that Afamin, a protein that has a gene sequence located on the same chromosome as Alpha-fetoprotein, may compensate for the absence of Alpha-fetoprotein during embryonic development. Nevertheless, research on the dynamics of Afamin expression and its correlation with Alpha-fetoprotein has not been reported. Therefore, it has been done a baseline study to determine the pattern and distribution of Alpha-fetoprotein expression and its correlation with Afamin expression in the developing rat liver. An analytic observational study was performed to study the expression of Afamin and Alpha-fetoprotein in the rat embryos (embryonic day/ED12.5, ED14.5, ED16.5, ED18.5), neonates and adults using an immunohistochemistry technique by assessing the location and intensity of expression using the Immunohistochemistry Optical density score. Afamin started to express in ED18.5 and was evenly distributed in the hepatocytes and was maintained until adulthood. Whereas, Alpha-fetoprotein has been seen at ED12.5 and was distributed evenly in the hepatoblast. At ED18.5, Alpha-fetoprotein expression reached a peak and decreased dramatically after birth. Spearman correlation test showed that both proteins' expressions were correlated in the opposite direction (P<0.05 and r =-0.695). In conclusion, Afamin and Alpha-fetoprotein have an opposite expression during development. The time point of intersection was ED18.5; implying the peak of hepatoblast proliferation to enter the differentiation process.
- Liver Development