The cytoskeleton protein β-actin may mediate T cell apoptosis during acute rejection reaction after liver transplantation in a rat model

Cytoskeletal proteins and associated regulatory proteins are essential for maintaining cell structure and growth. beta-actin is a major component of the cytoskeleton, and beta-actin remodeling is involved in lymphocyte migration, infiltration and apoptosis. However, little is known about whether changes in beta-actin expression affect lymphocyte cell fate, particularly during acute rejection after liver transplantation in a rat model. In our studies, grafts were harvested on days 5, 7 or 9 after xenogeneic rat liver transplantation. The acute rejection grade was histopathologically evaluated. Recipient-derived CD8(+) T lymphocytes gradually infiltrated into liver allografts in cases of severe acute rejection. The apoptotic rate of CD8(+) T lymphocytes peaked on day 7 and then decreased. Moreover, changes in beta-actin expression were consistent with the apoptotic rate of CD8(+) T lymphocytes in both allografts and peripheral blood based on western blotting and immunohistochemistry results. Additionally, jasplakinolide (an actin-stabilizing drug) evoked CD8(+) T lymphocyte apoptosis. In conclusion, our study is the first to describe the fluctuating expression levels and dynamics of the cytoskeletal protein beta-actin and its potential roles in the pathogenesis of acute rejection following rat liver transplantion. Our results enhance the understanding of the roles of CD8(+) T lymphocytes during acute rejection and suggest that beta-actin regulation leads to apoptosis.