Fig. 4: Albumin promoted exosomes secretion via Rab27a and induced TECs injury as a paracrine or autocrine signal.

a, b Rab27a knockdown by siRNA transfection in the presence of BSA. Rab27a was efficiently knockdown at mRNA and protein level. *p < 0.05 vs TECs transfected with NC. c, d Quantification of exosomes isolated from cultured supernatant of TECs. Knockdown of Rab27a significantly reduced exosome secretion as detected by western blotting analysis of exosomal markers (Alix, CD63, and CD81) (c) and EXOCET assay (d). **p < 0.01, ****p < 0.0001 vs TECs transfected with NC. e Exosomes isolated from TECs exposed to different doses of BSA were applied to naïve TECs. The mRNA expression of inflammatory cytokine (MCP-1, TNF-α, and IL-6) and tubular injury markers (KIM-1 and LCN2) in exosome-treated TECs are normalized to GAPDH and compared with Ctrl-exosomes-treated TECs (represented by 1-fold). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 vs TECs treated with Ctrl TEC-exo. f Expression of inflammatory cytokine and tubular injury marker in Rab27a knockdown-TECs in the presence of BSA are normalized to GAPDH and compared with NC-transfected TECs with BSA treatment (represented by 1-fold). **p < 0.01, ***p < 0.001 vs TECs transfected with NC. NC, negative control. Data presented as mean ± S.E.M. of three independent experiments.