Fig. 6
A schematic diagram of the protective role of pericytes in sepsis. After sepsis, pericyte desquamation, increased expression of endothelial S1PR2 and decreased ZO-1 and VE-cadherin are associated with vascular endothelial barrier breakdown; increased expression of S1PR1 and decreased p-MLC20 in VSMCs are associated with the vascular hyporeactivity. After pericyte transplantation, pericytes colonize in the mesenteric vein and form direct contact with endothelial cells to form a gap junction. Pericytes also secreted microvesicles (MVs) containing miR-145/132 to VSMCs and VECs to produce additional protective effects. miR-145 mainly acts on VSMCs to improve the vascular reactivity via inhibiting the expression of Sphk2 and S1PR1, and increasing the expression of p-MLC20. miR-132 mainly acts on VECs to improve the barrier function via inhibiting the expression of Sphk2 and S1PR2, and increasing the expression of ZO-1 and VE-cadherin. PC pericyte, PCMV pericyte-derived microvesicle, VEC vascular endothelial cell, VSMC vascular smooth muscle cell, p-MLC20 phosphorylation of myosin light chain 20, Sphk2 sphingosine kinase 2, S1PR1 sphingosine-1-phosphate receptor 1, ZO-1 zonula occludens-1, VE-cadherin vascular endothelial cadherin