Role of autophagy and evaluation the effects of microRNAs 214, 132, 34c and prorenin receptor in a rat model of focal segmental glomerulosclerosis

Focal segmental glomerulosclerosis (FSGS) is the common cause of chronic renal disease worldwide. Although there are many etiologic factors which have theme podocyte injury conclusive etiology not clearly understood. In this study, we aimed to explore role autophagy in pathogenesis injury, key point progression, and roles intrarenal microRNAs prorenin receptor (PRR) 5/6 nephrectomy adriamycin nephropathy models FSGS. For experimental FSGS model, were created characterized adult Sprague Dawley rats. Microarray analysis was performed on control groups that confirmed by q-RT-PCR. Beclin1, LC3B, PRR, ATG7 ATG5 expression evaluated western blotting immunohistochemistry. Also, Beclin1 PRR measured ELISA. Glomerular isolation autophagic activity podocytes before after transfection with miRNA mimic antagonists. significantly lower than group both when compared groups. Western blot results consistent immunohistochemical data. Electron microscopy revealed signs impaired Autophagic decreased miR-214, miR-132 miR-34c mimics increased These showed miR-34c, miR-214 could be a potential treatment strategy regulating autophagy.