Fig. 8: Transport mechanism. | Cell Death & Disease

Fig. 8: Transport mechanism.

From: HNRNPA1-mediated exosomal sorting of miR-483-5p out of renal tubular epithelial cells promotes the progression of diabetic nephropathy-induced renal interstitial fibrosis

Fig. 8

A Mechanism flow diagram. Under physiological conditions (non diabetic), most miR-483 (miR-483-5p) remained in the renal tubular epithelial cells, and only a small amount of miR-483 was encapsulated into MVB (multivesicular body, vesicles) and was secreted into the extracellular through exosomes. Therefore, the intracellular miR-483 blocked ECM synthesis by restraining the TIMP2/MAPK1 pathway; Under pathological conditions, most miR-483 was encapsulated into MVB and was secreted into the extracellular domain through exosomes and transferred into the urine. Therefore, miR-483 was highly expressed in the urinary exosomes, and the lack of miR-483 in renal tubular epithelial cells led to the activation of the TIMP2/MAPK1 pathway, thus promoting ECM synthesis. B Pearson correlation coefficient analysis of the correlation between urinary ACR and urinary exosome miR-483-5p. Pearson correlation coefficient analysis of three independent experiments.

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