scholarly journals CircHIPK3 Alleviates High Glucose Toxicity to Human Renal Tubular Epithelial HK-2 Cells Through Regulation of miR-326/miR-487a-3p/SIRT1

2021 ◽  
Vol Volume 14 ◽  
pp. 729-740
Author(s):  
Langen Zhuang ◽  
Ziwei Wang ◽  
Xiaolei Hu ◽  
Qingqing Yang ◽  
Xiaoyan Pei ◽  
...  
Keyword(s):  
High Glucose ◽  
Glucose Toxicity ◽  
Renal Tubular

scholarly journals Silence of lncRNA GAS5 alleviates high glucose toxicity to human renal tubular epithelial HK-2 cells through regulation of miR-27a

2019 ◽  
Vol 47 (1) ◽  
pp. 2205-2212 ◽  
Author(s):  
Lina Lv ◽  
Dandan Li ◽  
Fengqun Tian ◽  
Xia Li ◽  
Jing Zhang ◽  
...  
Keyword(s):  
High Glucose ◽  
Glucose Toxicity ◽  
Renal Tubular ◽  
Lncrna Gas5

scholarly journals CD36 promotes NLRP3 inflammasome activation via the mtROS pathway in renal tubular epithelial cells of diabetic kidneys

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Yanjuan Hou ◽  
Qian Wang ◽  
Baosheng Han ◽  
Yiliang Chen ◽  
Xi Qiao ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
High Glucose ◽  
Inflammasome Activation ◽  
Ros Production ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Nlrp3 Inflammasome Activation ◽  
Ampk Activity ◽  
Renal Tubular ◽  
Tubulointerstitial Inflammation

AbstractTubulointerstitial inflammation plays a key role in the pathogenesis of diabetic nephropathy (DN). Interleukin-1β (IL-1β) is the key proinflammatory cytokine associated with tubulointerstitial inflammation. The NLRP3 inflammasome regulates IL-1β activation and secretion. Reactive oxygen species (ROS) represents the main mediator of NLRP3 inflammasome activation. We previously reported that CD36, a class B scavenger receptor, mediates ROS production in DN. Here, we determined whether CD36 is involved in NLRP3 inflammasome activation and explored the underlying mechanisms. We observed that high glucose induced-NLRP3 inflammasome activation mediate IL-1β secretion, caspase-1 activation, and apoptosis in HK-2 cells. In addition, the levels of CD36, NLRP3, and IL-1β expression (protein and mRNA) were all significantly increased under high glucose conditions. CD36 knockdown resulted in decreased NLRP3 activation and IL-1β secretion. CD36 knockdown or the addition of MitoTempo significantly inhibited ROS production in HK-2 cells. CD36 overexpression enhanced NLRP3 activation, which was reduced by MitoTempo. High glucose levels induced a change in the metabolism of HK-2 cells from fatty acid oxidation (FAO) to glycolysis, which promoted mitochondrial ROS (mtROS) production after 72 h. CD36 knockdown increased the level of AMP-activated protein kinase (AMPK) activity and mitochondrial FAO, which was accompanied by the inhibition of NLRP3 and IL-1β. The in vivo experimental results indicate that an inhibition of CD36 could protect diabetic db/db mice from tubulointerstitial inflammation and tubular epithelial cell apoptosis. CD36 mediates mtROS production and NLRP3 inflammasome activation in db/db mice. CD36 inhibition upregulated the level of FAO-related enzymes and AMPK activity in db/db mice. These results suggest that NLRP3 inflammasome activation is mediated by CD36 in renal tubular epithelial cells in DN, which suppresses mitochondrial FAO and stimulates mtROS production.

Transcriptome alterations in high glucose-induced renal tubular cells of bactrian camel

2020 ◽  
Vol 27 (3) ◽  
pp. 301-304
Author(s):  
Bin Yang ◽  
Lihui Chen ◽  
Xin Li ◽  
Zhuwei Guo ◽  
Shi Liu ◽  
...  
Keyword(s):  
High Glucose ◽  
Bactrian Camel ◽  
Tubular Cells ◽  
Renal Tubular 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
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