Fig. 4

PCMVs regulate the contractile response of VSMCs and barrier function of VECs after sepsis. a Identification of PCMV. (i-ii) Representative TEM micrographs of microvesicle isolated from pericyte; (iii) Representative SEM micrographs of microvesicle observed from pericytes; (iv) PCMV diameter measured by DLS analysis. b Role of PCMVs and Poly(I:C)PCMVs (2 × 10⁶ microvesicles/ml) on the contractile response of rat VSMC to NE at 12 h after LPS (2 μg/ml) stimulation (n = 8 cells). c Role of PCMVs and Poly(I:C)PCMVs on the barrier function of rat VECs after LPS administration. i PCMVs and Poly(I:C)PCMVs were added into rat VECs, and TEER of each group was measured (n = 3 cells); ii PCMVs and Poly(I:C)PCMVs were added into VECs, and FITC–BSA penetration of each group was measured (n = 8 cells); iii VECs treated with PCMV were analyzed by immunofluorescence for ZO-1. Scale bars: 20 μm. d Changes in vascular response of mesenteric arterioles to NE and Ach in vivo after PCMV transplantation (n = 8 rats). Scale bars: 50 μm. e Vascular leakage of mesenteric venules measured after PCMV transplantation (n = 8 rats). Scale bars: 50 μm. PC pericyte, PCMV pericyte-derived microvesicle, TEM transmission electron microscopy, SEM scanning electron microscopy, VECs vascular endothelial cells, VSMCs vascular smooth muscle cells, LPS lipopolysaccharides, TEER transendothelial electrical resistance, ZO-1 zonula occludens-1, NE norepinephrine, Ach acetylcholine, MA mesenteric arteriole. Data shown as mean ± SD. ^**P < 0.01, ^***P < 0.001 vs. Normal control or Sham; ^##P < 0.01, ^###P < 0.001 vs. LPS or Sepsis (one-way ANOVA)