Authors:

Mitchell Taylor

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About Paper:

Chronic liver diseases arise from repeated cycles of injury/repair and are characterized by impaired cell proliferation through poorly understood mechanisms. Yes-associated protein 1 (YAP), a transcriptional co-activator that partners with Tead transcription factors, regulates cell proliferation and is activated in conditions like metabolic-associated fatty liver disease and steatohepatitis. Although YAP is transiently activated to promote liver regeneration after injury, the long-term effects of repeated YAP activation on cell proliferation capacity remain unclear. Using an inducible YAP mouse model, we investigated whether repeated cycles of transient YAP activation impair proliferative capacity. We found that liver size did not differ significantly after multiple cycles of YAP activation. The number of Hn4a+ hepatocytes remained stable across these cycles, indicating that homeostatic balance was maintained. Additionally, the expression of the cell proliferation marker Mki67 remained responsive to YAP activation. However, immunofluorescence analysis revealed decreased Ki67+ proliferating cells after repeated YAP cycles, suggesting post-transcriptional regulation of cell proliferation through Ki67. These findings provide insight into how proliferative capacity becomes compromised during the injury-repair cycles that characterize chronic liver disease progression. Future studies will investigate the mechanisms linking repeated YAP activation to Ki67 protein regulation.

Source:

Auburn University / College of Sciences and Mathematics / 2025

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Co-authors:

Mitchell Taylor