Silencing of LncRNA TCONS_00088786 reduces renal fibrosis through miR-132

S.-G. Zhou, W. Zhang, H.-J. Ma, Z.-Y. Guo, Y. Xu

Department of Nephrology, Jining No. 1 People’s Hospital, Jining, China. Xuyan1101396@sohu.com

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• Nephrology

OBJECTIVE: To examine the role of long non-coding ribonucleic acid (LncRNA) TCONS_00088786 in the development of renal interstitial fibrosis and its potential mechanism in this process.

MATERIALS AND METHODS: Unilateral ureteral obstruction (UUO) was used to induce tubulointerstitial fibrosis. Masson staining showed the degree of renal fibrosis in UUO mice. Immunohistochemistry and immunofluorescence were performed to detect the fibrosis-related proteins, the 24-h urine volume and protein content. The renal functions were reflected via serum creatinine (Scr) and blood urea nitrogen (BUN). Changes in lncRNATCONS_00088786, miR-132 and collagen I and III in the development process of renal fibrosis were detected through reverse transcription-polymerase chain reaction (RT-PCR). Small interfering RNA (siRNA) was transfected into NRK52E cells to mimic the knockdown. Western blot was adopted to detect the changes in miR-132, collagen I and III after the siRNA was transfected by transforming growth factor-β (TGF-β) for 24 h.

RESULTS: With the development of renal fibrosis, lncRNA TCONS_00088786 and miR-132 were increased gradually. After the knockdown of lncRNA TCONS_00088786, miR-132 was decreased and fibrosis-related protein was also decreased.

CONCLUSIONS: Decreased lncRNA TCONS _00088786 inhibits renal interstitial fibrosis by reducing miR-132 and it may be a potential novel molecular target for the treatment of renal interstitial fibrosis.

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