M2 macrophage ‐derived exosomal miR‐25‐3p improves high glucose‐induced podocytes injury through activation autophagy via inhibiting DUSP1 expression

AbstractDiabetic nephropathy (DN) is the primary reason of chronic kidney disease. The aim of our study is to explore the role and action mechanism of M2 macrophage ‐derived exosomes in high glucose (HG)‐induced podocytes injury. Here, 30 mmol/L of HG was used to induce podocytes injury. Annexin V‐FITC/PI double staining was performed to measure podocytes apoptosis, and western blot was carried out to ensure proteins expression. The shape of exosomes wa s identified using TEM. Besides, the expression of miR‐25‐3p was determined by qRT‐PCR, FAM‐labeled miR‐25‐5p combined with DiI‐labeled exosomes were utilized to explore the uptake of podocytes to exosomes. Relationship between miR‐25‐3p and DUSP family members was ensued by lucife rase activity assay. In the beginning, we found that M2 macrophage ameliorated HG‐induced podocytes apoptosis and epithelial‐mesenchymal transition through secreting exosomes. Subsequently, highly expressed miR‐25‐3p was found in M2 macrophage‐derived exosomes that effectively improved HG‐ induced podocytes injury. Furthermore, inhibition of miR‐25‐3p in M2 macrophage inefficiently repressed HG‐induced podocytes injury, thus we proposed that M2 macrophage attenuated podocytes injury through secreting exosomal miR‐25‐3p. Then, we used an autophagy inhibitor to stimulate podoc ytes, and demonstrated that M2 macrophage‐derived exosomal miR‐25‐3p improved HG‐induced podocytes injury through activat...
Source: IUBMB Life - Category: Research Authors: Tags: RESEARCH COMMUNICATION Source Type: research