| First Author | Apte U | Year | 2007 |
| Journal | Am J Physiol Gastrointest Liver Physiol | Volume | 292 |
| Issue | 6 | Pages | G1578-85 |
| PubMed ID | 17332475 | Mgi Jnum | J:123695 |
| Mgi Id | MGI:3719303 | Doi | 10.1152/ajpgi.00359.2006 |
| Citation | Apte U, et al. (2007) beta-Catenin is critical for early postnatal liver growth. Am J Physiol Gastrointest Liver Physiol 292(6):G1578-85 |
| abstractText | The Wnt/beta-catenin pathway plays an important role in embryonic liver development, morphogenesis, and organogenesis. Here, we report on the activation of beta-catenin during early postnatal liver growth. Modulation of beta-catenin expression was studied in CD-1 mice livers over a time course of 0 to 30 postnatal days (PD) and 3 mo. Increases in total and active beta-catenin were observed in developing livers from PD 5 to 20. A concomitant increase in the beta-catenin-transcription factor (TCF) complex along with nuclear and cytoplasmic beta-catenin was also evident, which coincided with ongoing hepatocyte proliferation by PCNA immunohistochemistry. This activation of beta-catenin was multifactorial, including cyclical inhibition of glycogen synthase kinase-3beta, suppression of casein kinase-IIalpha, and a transient increase in beta-catenin gene expression. Coprecipitation experiments revealed the formation of the beta-catenin-cadherin complex at PD 5, whereas adequate beta-catenin-c-Met complex at the hepatocyte membrane did not form until PD 20, which might be contributing to the free beta-catenin pool during early postnatal growth. Furthermore, beta-catenin liver-specific knockout mice exhibited smaller livers at PD 30, secondary to diminished hepatocyte proliferation. These data indicate that the activation of beta-catenin is critical for early postnatal liver growth and development. |
