scholarly journals (−)-Epicatechin and the colonic metabolite 2,3-dihydroxybenzoic acid protect against high glucose and lipopolysaccharide-induced inflammation in renal proximal tubular cells through NOX-4/p38 signalling

2020 ◽  
Vol 11 (10) ◽  
pp. 8811-8824
Author(s):  
David Álvarez Cilleros ◽  
María Elvira López-Oliva ◽  
María Ángeles Martín ◽  
Sonia Ramos
Keyword(s):  
Kidney Disease ◽  
High Glucose ◽  
Diabetic Kidney Disease ◽  
Dihydroxybenzoic Acid ◽  
Proximal Tubular Cells ◽  
Tubular Cells ◽  
Proximal Tubular ◽  
Renal Proximal Tubular Cells ◽  
Renal Proximal Tubular ◽  
Chronic Hyperglycaemia

Chronic hyperglycaemia and inflammation are present in diabetes and both processes have been related to the pathogenesis of diabetic kidney disease.

Possible involvement of intracellular angiotensin II receptor in high-glucose-induced damage in renal proximal tubular cells

2010 ◽  
Vol 24 (2) ◽  
pp. 218-224 ◽  
Author(s):  
Toshihiro Takao ◽  
Taro Horino ◽  
Toru Kagawa ◽  
Reiko Matsumoto ◽  
Yoshiko Shimamura ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
High Glucose ◽  
Angiotensin Ii Receptor ◽  
Proximal Tubular Cells ◽  
Tubular Cells ◽  
Proximal Tubular ◽  
Renal Proximal Tubular Cells ◽  
Renal Proximal Tubular

scholarly journals Mechanisms through which high glucose concentration raises [Ca2+]i in renal proximal tubular cells

1998 ◽  
Vol 54 (4) ◽  
pp. 1206-1213 ◽  
Author(s):  
Margarita Symonian ◽  
Miroslaw Smogorzewski ◽  
Wojciech Marcinkowski ◽  
Ewa Krol ◽  
Shaul G. Massry
Keyword(s):  
High Glucose ◽  
Glucose Concentration ◽  
High Glucose Concentration ◽  
Proximal Tubular Cells ◽  
Tubular Cells ◽  
Proximal Tubular ◽  
Renal Proximal Tubular Cells ◽  
Renal Proximal Tubular

scholarly journals Reactive oxygen species blockade and action of insulin on expression of angiotensinogen gene in proximal tubular cells

2004 ◽  
Vol 183 (3) ◽  
pp. 535-550 ◽  
Author(s):  
Tusty-Jiuan Hsieh ◽  
Pierre Fustier ◽  
Chih-Chang Wei ◽  
Shao-Ling Zhang ◽  
Janos G Filep ◽  
...  
Keyword(s):  
High Glucose ◽  
Diabetic Rat ◽  
Ros Generation ◽  
Ang Ii ◽  
Proximal Tubular Cells ◽  
Tubular Cells ◽  
Gf 109203X ◽  
Proximal Tubular ◽  
Renal Proximal Tubular Cells ◽  
Renal Proximal Tubular

We reported previously that insulin inhibits the stimulatory effect of high glucose on the expression of angiotensinogen (ANG) gene in both rat immortalized renal proximal tubular cells (IRPTCs) and non-diabetic rat renal proximal tubular cells (RPTCs), but has no effect in diabetic rat RPTCs. In the present study we investigated whether hyperglycaemia-induced resistance to the insulin-induced inhibition of expression of the ANG gene is mediated via the generation of reactive oxygen species (ROS) in RPTCs. Rat IRPTCs were cultured for 2 weeks in high-glucose (25 mM) or normal-glucose (5 mM) medium plus angiotensin II (Ang II) with or without a superoxide scavenger (tiron), or inhibitors of: NADPH oxidase (diphenylene iodinium, DPI), Ang II type 1 and 2 receptors (losartan and PD123319), angiotensin-converting enzyme (perindopril), protein kinase C (GF 109203X), or glutamine:fructose-6-phosphate amino-transferase (azaserine). Cellular generation of ROS, and ANG and renin mRNA levels were assessed by lucigenin assay and specific reverse transcriptase-PCR respectively. Phosphorylation of p44/42 mitogen-activated protein kinase (p44/42 MAPK) was evaluated by western blotting. Prolonged exposure of IRPTCs to high concentrations of glucose or Ang II evoked generation of ROS and resistance to the insulin-induced inhibition of expression of the ANG gene and of p44/42 MAPK phosphorylation. Co-incubation of IRPTCs with tiron, DPI, losartan, PD123319, perindopril, GF 109203X or azaserine prevented ROS generation, restoring the inhibitory action of insulin on ANG gene expression and on p44/42 MAPK phosphorylation. In conclusion, our studies demonstrate that blockade of both ROS generation and activation of the intrarenal renin–angiotensin system improves the inhibitory action of insulin on ANG gene expression in IRPTCs in conditions of high glucose.

scholarly journals High glucose augments angiotensinogen in human renal proximal tubular cells through hepatocyte nuclear factor-5

PLoS ONE ◽  
2017 ◽  
Vol 12 (10) ◽  
pp. e0185600 ◽  
Author(s):  
Juan Wang ◽  
Yuki Shibayama ◽  
Hiroyuki Kobori ◽  
Ya Liu ◽  
Hideki Kobara ◽  
...  
Keyword(s):  
High Glucose ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Proximal Tubular Cells ◽  
Tubular Cells ◽  
Proximal Tubular ◽  
Renal Proximal Tubular Cells ◽  
Renal Proximal Tubular

scholarly journals Essential Role(s) of the Intrarenal Renin-Angiotensin System in Transforming Growth Factor–β1 Gene Expression and Induction of Hypertrophy of Rat Kidney Proximal Tubular Cells in High Glucose

2002 ◽  
Vol 13 (2) ◽  
pp. 302-312
Author(s):  
Shao-Ling Zhang ◽  
Catherine To ◽  
Xing Chen ◽  
Janos G. Filep ◽  
Shiow-Shih Tang ◽  
...  
Keyword(s):  
Gene Expression ◽  
High Glucose ◽  
Transforming Growth Factor ◽  
Proximal Tubular Cells ◽  
Tubular Cells ◽  
Type Iv ◽  
Proximal Tubular ◽  
Renal Proximal Tubular Cells ◽  
Renal Proximal Tubular ◽  
Tgf Β1

ABSTRACT. These studies investigated the question of whether the intrarenal renin-angiotensin system (RAS) is essential for transforming growth factor–β1 (TGF-β1) gene expression and induction of hypertrophy of renal proximal tubular cells in high glucose in vitro. Antisense and sense angiotensinogen (ANG) cDNAs were stably transfected into rat immortalized renal proximal tubular cells (IRPTC). ANG secretion from rat IRPTC was quantified by a specific RIA for rat ANG. Cellular ANG, TGF-β1, and collagen α1 (type IV) mRNA levels were determined by Northern blot analysis or by reverse transcriptase–PCR assay. Hypertrophy of IRPTC was analyzed by Western blotting of cellular p27Kip1 protein, flow cytometry, and cellular protein assay. The results showed that stable transfer of antisense ANG cDNA into IRPTC suppressed the basal TGF-β1 and collagen α1 (type IV) mRNA expression and blocked the stimulatory effect of high glucose (i.e., 25 mM) on TGF-β1 and collagen α1 (type IV) mRNA expression and induction of IRPTC hypertrophy. In contrast, stable transfer of sense ANG cDNA into IRPTC had no significant effect on these parameters. These data demonstrate that local intrarenal RAS activation is essential for TGF-β1 gene expression and induction of hypertrophy of renal proximal tubular cells in high glucose.

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