To investigate the expression of long noncoding RNA (lncRNA) LINC00261 in diabetic nephropathy and its possible protective effect on HK-2 cells in high glucose environment through the microRNA miR-148b-3p/PTEN pathway.

From March 2016 to May 2018, 19 patients with diabetic nephropathy and 23 healthy controls from our hospital were selected. The blood samples were collected, and the expressions of LINC00261 and miR-148b-3p were determined by quantitative real-time PCR (qRT-PCR). In cell experiments, the HK-2 renal tubular epithelial cells were divided into 7 groups: NG group with normal glucose (5.5 mmol/L), HG group with high glucose (30.0 mmol/L), and the other 5 groups were all with high glucose : pcDNA group (empty plasmid transfection), LINC00261 group (pcDNA-LINC00261 transfection), anti-miR-NC group (negative control transfection), anti-miR-148b-3p group (inhibitor transfection), and LINC0026+ miR-148b-3p group (transfection of pcDNA-LINC00261 and miR-148b-3p). The expression of PTEN protein, cell proliferation, and apoptosis were detected by western blotting, cell counting kit 8, and flow cytometry, respectively. Superoxide dismutase (SOD) kit and malondialdehyde (MDA) kit were used to detect SOD activity and MDA content, respectively. The dual luciferase reporter assay was used to identify the relationship among LINC00261, miR-148b-3p, and PTEN.

Compared with healthy controls, the expression of LINC00261 in patients with diabetic nephropathy was significantly decreased, while the expression of miR-148b-3p was apparently increased (P<0.05). After overexpression of LINC00261 or inhibition of miR-148b-3p, the expression of miR-148b-3p, apoptosis, and MDA of HK-2 cells in high glucose environment were all decreased, but the PTEN protein expression, cell proliferation, and SOD activity were all increased (P<0.05).

LINC00261 may promote the proliferation, relieve oxidative stress, and decrease apoptosis of HK-2 renal tubular epithelial cells in high glucose environment through regulating the miR-148b-3p/PTEN pathway.