RESUMO
Renal fibrosis is a common pathological feature of chronic kidney diseases, and their development and progression are influenced by epigenetic modifications including aberrant microRNA (miRNA or miR) expression. miRNAs have been demonstrated to modulate the aggressiveness of various cancers and have emerged as possible therapeutic agents for the management of renal fibrosis. Transforming growth factor ß1 (TGFß1)induced epithelialmesenchymal transition (EMT) of tubular epithelial cells serves a role in the initiation and progression of renal fibrosis. Furthermore, recent results indicated that the progression of EMT is reversible. The present study aimed to clarify the role of miR152 in EMT of the tubular epithelial cell line HK2, stimulated by TGFß1, using in vitro transfection with a miR152 mimic and to further investigate the underlying mechanism of miR152 activity. In the present study, miR152 expression was significantly reduced in TGFß1treated HK2 cells, accompanied by an increased expression of hematopoietic preBcell leukemia transcription factor (PBX)interacting protein (HPIP). Additionally, miR152 overexpression inhibited TGFß1induced EMT and suppressed HPIP expression by directly targeting the 3' untranslated region of HPIP in HK2 cells. Furthermore, upregulation of HPIP reversed miR152mediated inhibitory effects on the EMT. Collectively, the results suggest that downregulation of miR152 initiates the dedifferentiation of renal tubules and progression of renal fibrosis, which may provide important targets for prevention strategies of renal fibrosis.