Figure 1
From: Platelets prime hematopoietic–vascular niche to drive angiocrine-mediated liver regeneration

Hepatotoxic injury recruits CD41+ platelets carrying VEGF-A and SDF-1 to liver vasculature. (a, b) After intraperitoneal (i.p.) injection of hepatotoxic agent carbon tetrachloride (CCl4), CD41+ platelets expressing VEGF-A and SDF-1 were recruited to VEGFR3+ liver sinusoidal endothelial cells (LSECs). Liver sections were stained with antibodies against platelet marker CD41, VEGF-A (a), SDF-1 (b) and LSEC-specific marker VEGFR3. After CCl4 injury, but not administration of PBS (control), CD41+SDF-1+VEGF-A+ platelets were associated with VEGFR3+ LSECs; scale bar, 50 μm. (c) Quantification of CD41+SDF-1+VEGF-A+ platelets associated with VEGFR3+ LSECs. N=5–7 mice per group. (d) Flow cytometry analysis of platelet accumulation in the CCl4-injured and control livers. Activation of CD41+ platelets was evidenced by surface expression of activation marker P-selectin.