Fig. 7From: Early severe impairment of hematopoietic stem and progenitor cells from the bone marrow caused by CLP sepsis and endotoxemia in a humanized mice modelEffects of Notch pathway inhibition in human HSPCs 24 h after induction of CLP sepsis in hu-mice. Pretreatment with DAPT (60 mg/kg) 2 h before CLP surgery inhibited activation of Notch-1 assessed by fluorescence intensity of NICD (a). Impact of the inhibition of Notch signaling on the CLP-induced expansion of CD34+ CD38− HSCs (b, c) and effect on CD34+ CD38+ progenitors (d, e). Influence of DAPT treatment on the frequency of proliferating HSCs (f), and the rate of apoptosis of CD34+ CD38− cells (g). Effect of DAPT on the expression of G-CSFR on HSPCs after CLP (h), and the phosphorylation of STAT3 (i). n = 3–5. *P < 0.05, **P < 0.001, ***P < 0.001. CLP cecum ligation and puncture, G-CSFR granulocyte colony-stimulating factor receptor, GMF geometric mean fluorescence, HSC hematopoietic stem cell, HSPC hematopoietic stem and progenitor cell, NICD Notch-1 intracellular domainBack to article page