Long non-coding RNAs (lncRNAs) are important regulators in
diabetic nephropathy. In this study, we investigated the potential role of
lncRNA TUG1 in regulating endoplasmic reticulum stress (ERS)-mediated apoptosis in high
glucose induced renal tubular epithelial cells. Human renal tubular epithelial cell line HK-2 was challenged with high
glucose following transfection with
lncRNA TUG1, miR-29c-3p mimics or inhibitor expression plasmid, either alone or in combination, for different experimental purposes. Potential binding effects between TUG1 and miR-29c-3p, as well as between miR-29c-3p and
SIRT1 were verified. High
glucose induced apoptosis and ERS in HK-2 cells, and significantly decreased TUG1 expression. Overexpressed TUG1 could prevent high
glucose-induced apoptosis and alleviated ERS via negatively regulating miR-29c-3p. In contrast, miR-29c-3p increased HK-2 cells apoptosis and ERS upon high
glucose-challenge.
SIRT1 was a direct target gene of miR-29c-3p in HK-2 cells, which participated in the effects of miR-29c-3p on HK-2 cells. Mechanistically, TUG1 suppressed the expression of miR-29c-3p, thus counteracting its function in downregulating the level of
SIRT1. TUG1 regulates miR-29c-3p/
SIRT1 and subsequent ERS to relieve high
glucose induced renal epithelial cells injury, and suggests a potential role for TUG1 as a promising diagnostic marker of
diabetic nephropathy.