Smad Anchor for Receptor Activation Regulates High Glucose-Induced EMT via Modulation of Smad2 and Smad3 Activities in Renal Tubular Epithelial Cells

Nephron ◽  
2015 ◽  
Vol 130 (3) ◽  
pp. 213-220 ◽  
Author(s):  
Wen-bin Tang ◽  
Guang-hui Ling ◽  
Lin Sun ◽  
Ke Zhang ◽  
Xuejing Zhu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
High Glucose ◽  
Receptor Activation ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Renal Tubular

scholarly journals Nox4 is involved in high glucose-induced apoptosis in renal tubular epithelial cells via Notch pathway

2017 ◽  
Vol 15 (6) ◽  
pp. 4319-4325 ◽  
Author(s):  
Min Yao ◽  
Feng Gao ◽  
Xiaomeng Wang ◽  
Yonghong Shi ◽  
Shuxia Liu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
High Glucose ◽  
Notch Pathway ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Renal Tubular ◽  
Induced Apoptosis

scholarly journals Knockdown of the Long Noncoding RNA LUCAT1 Inhibits High-Glucose-Induced Epithelial-Mesenchymal Transition through the miR-199a-5p–ZEB1 Axis in Human Renal Tubular Epithelial Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Li-Cai Zhang ◽  
Zong-Bin Wei ◽  
Shui-Fu Tang
Keyword(s):  
Epithelial Cells ◽  
High Glucose ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Epithelial Mesenchymal Transition ◽  
Negative Control ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Mesenchymal Transition ◽  
Renal Tubular

Renal fibrosis, the leading cause of end-stage renal disease and in which epithelial-mesenchymal transition (EMT) plays a central role, has a complex pathogenesis that is not fully understood. Therefore, we investigated the role of the long noncoding RNA LUCAT1 in the EMT of renal tubular epithelial cells under high-glucose (HG) conditions and the underlying mechanism involved. In this study, we established HG and normal glucose groups of HK-2 cells by treating HK-2 cells 30.0 or 5.5 mmol/L glucose, respectively. To investigate the roles of LUCAT1 and miR-199a-5p in HG-induced EMT, we transfected the HG group with negative control small interfering RNA (siRNA), siRNA targeting LUCAT1, negative control microRNA, or an miR-199a-5p mimic. The results of the quantitative reverse transcription PCR indicated that the LUCAT1 level in the HG group was increased, whereas the miR-199a-5p level was decreased. The EMT in the cells was induced by treatment with HG but was weakened by LUCAT1 knockdown or miR-199a-5p overexpression, which both also inhibited the HG-induced phosphorylation of SMAD3. Moreover, LUCAT1 and ZEB1 mRNA comprised the same microRNA response elements of miR-199a-5p. LUCAT1 knockdown had no effect on the miR-199a-5p level but decreased the HG-induced upregulation of ZEB1. In conclusion, HG conditions induced the upregulation of LUCAT1, and LUCAT1 knockdown inhibited the EMT in HG-treated HK-2 cells. LUCAT1 likely promotes HG-induced EMT through ZEB1 by sponging miR-199a-5p.

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