Figure 2 | Signal Transduction and Targeted Therapy

Figure 2

From: Platelets prime hematopoietic–vascular niche to drive angiocrine-mediated liver regeneration

Figure 2

Platelet-deficient mice exhibit impaired liver regeneration after CCl4 injury. (a, b) After CCl4 injury, proliferation (BrdU+) of hepatocytes was prohibited in thrombopoietin knockout mice (Thpo−/−) lacking platelets. Hepatocyte proliferation was enhanced in Thpo−/− mice by injection of VEGF-A and SDF-1. N=6–8 mice per group. (c) Severe centrilobular damage in the liver of Thpo−/− mice after CCl4 injury, as indicated by scattered cell debris in Thpo−/− mice relative to mild centrilobular necrosis in WT mice. VEGF-A and SDF-1 injection ameliorated the injury in Thpo−/− mice. Scale bar, 50 μm. (d) Increased hepatic injury (plasma alanine aminotransferase, ALT activity) in Thpo−/− mice following CCl4 injection, as compared to WT mice. These data imply that VEGF-A and SDF-1 produced by activated platelets protect against acute hepatotoxic injury. N=6–8 mice per group.

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