TGFbeta induces apoptosis and EMT in primary mouse hepatocytes independently of p53, p21Cip1 or Rb status
2008

TGFbeta induces cell death and changes in liver cells

publication 10 minutes Evidence: moderate

Author Information

Author(s): Sharon Sheahan, Christopher O. Bellamy, Stephen N. Harland, David J. Harrison, Sandrine Prost

Primary Institution: Queen's Medical Research Institute, University of Edinburgh

Hypothesis

How do p53, p21Cip1, and Rb deficiencies affect TGFβ-induced apoptosis and EMT in hepatocytes?

Conclusion

TGFβ induces apoptosis in hepatocytes regardless of p53, p21Cip1, and Rb status, but these proteins slightly modulate the process.

Supporting Evidence

  • TGFβ induces high levels of apoptosis in hepatocytes regardless of their genetic background.
  • Deficiencies in p53 and p21Cip1 decrease sensitivity to TGFβ-induced apoptosis.
  • TGFβ treatment leads to morphological changes in hepatocytes that are independent of p53, p21Cip1, and Rb status.

Takeaway

When liver cells are treated with a substance called TGFβ, they can die, and this happens no matter what genes they have. Some genes can change how sensitive the cells are to this treatment.

Methodology

Primary mouse hepatocytes were treated with TGFβ for 24 to 96 hours, and apoptosis was quantified using morphology and cleaved-caspase 3 immunostaining.

Limitations

The study primarily focuses on specific gene deficiencies and may not account for other factors influencing TGFβ responses.

Participant Demographics

Male mice, aged 6–12 weeks.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1186/1471-2407-8-191

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