scholarly journals Pioglitazone Attenuates Reoxygenation Injury in Renal Tubular NRK-52E Cells Exposed to High Glucose via Inhibiting Oxidative Stress and Endoplasmic Reticulum Stress

2020 ◽  
Vol 10 ◽  
Author(s):  
Cong Zou ◽  
Zhiyu Zhou ◽  
Yunming Tu ◽  
Weichao Wang ◽  
Tongchang Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
High Glucose ◽  
Reoxygenation Injury ◽  
Renal Tubular

scholarly journals LncRNA TUG1/miR-29c-3p/SIRT1 axis regulates endoplasmic reticulum stress-mediated renal epithelial cells injury in diabetic nephropathy model in vitro

PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0252761
Author(s):  
Shaoqiang Wang ◽  
Pengfei Yi ◽  
Na Wang ◽  
Min Song ◽  
Wenhui Li ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Diabetic Nephropathy ◽  
Epithelial Cells ◽  
Endoplasmic Reticulum Stress ◽  
High Glucose ◽  
Potential Role ◽  
Renal Epithelial Cells ◽  
Renal Tubular ◽  
Induced Apoptosis ◽  
Lncrna Tug1

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.

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