scholarly journals Retraction: Arg tyrosine kinase modulates TGF-β1 production in human renal tubular cells under high-glucose conditions

2020 ◽  
Vol 133 (20) ◽  
pp. jcs254847
Author(s):  
Barbara Torsello ◽  
Cristina Bianchi ◽  
Chiara Meregalli ◽  
Vitalba Di Stefano ◽  
Lara Invernizzi ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
High Glucose ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Arg Tyrosine Kinase ◽  
Renal Tubular ◽  
Tgf Β1

Correction: Arg tyrosine kinase modulates TGF-β1 production in human renal tubular cells under high-glucose conditions (doi:10.1242/jcs.183640)

2019 ◽  
Vol 132 (19) ◽  
pp. jcs238832
Author(s):  
Barbara Torsello ◽  
Cristina Bianchi ◽  
Chiara Meregalli ◽  
Vitalba Di Stefano ◽  
Lara Invernizzi ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
High Glucose ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Arg Tyrosine Kinase ◽  
Renal Tubular ◽  
Tgf Β1

scholarly journals Arg tyrosine kinase modulates TGF-β1 production in human renal tubular cells under high-glucose conditions

2016 ◽  
Vol 129 (15) ◽  
pp. 2925-2936 ◽  
Author(s):  
Barbara Torsello ◽  
Cristina Bianchi ◽  
Chiara Meregalli ◽  
Vitalba Di Stefano ◽  
Lara Invernizzi ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
High Glucose ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Arg Tyrosine Kinase ◽  
Renal Tubular ◽  
Tgf Β1

scholarly journals METTL14-regulated PI3K/Akt signaling pathway via PTEN affects HDAC5-mediated epithelial–mesenchymal transition of renal tubular cells in diabetic kidney disease

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Zhaoxia Xu ◽  
Keqi Jia ◽  
Hui Wang ◽  
Feng Gao ◽  
Song Zhao ◽  
...  
Keyword(s):  
Kidney Disease ◽  
High Glucose ◽  
Diabetic Kidney Disease ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Hk2 Cells ◽  
Tgf Β1

AbstractHistone deacetylase 5 (HDAC5) belongs to class II HDAC subfamily and is reported to be increased in the kidneys of diabetic patients and animals. However, little is known about its function and the exact mechanism in diabetic kidney disease (DKD). Here, we found that HDAC5 was located in renal glomeruli and tubular cells, and significantly upregulated in diabetic mice and UUO mice, especially in renal tubular cells and interstitium. Knockdown of HDAC5 ameliorated high glucose-induced epithelial–mesenchymal transition (EMT) of HK2 cells, indicated in the increased E-cadherin and decreased α-SMA, via the downregulation of TGF-β1. Furthermore, HDAC5 expression was regulated by PI3K/Akt signaling pathway and inhibition of PI3K/Akt pathway by LY294002 treatment or Akt phosphorylation mutation reduced HDAC5 and TGF-β1 expression in vitro high glucose-cultured HK2 cells. Again, high glucose stimulation downregulated total m6A RNA methylation level of HK2 cells. Then, m6A demethylase inhibitor MA2 treatment decreased Akt phosphorylation, HDAC5, and TGF-β1 expression in high glucose-cultured HK2 cells. In addition, m6A modification-associated methylase METTL3 and METTL14 were decreased by high glucose at the levels of mRNA and protein. METTL14 not METTL3 overexpression led to PI3K/Akt pathway inactivation in high glucose-treated HK2 cells by enhancing PTEN, followed by HDAC5 and TGF-β1 expression downregulation. Finally, in vivo HDACs inhibitor TSA treatment alleviated extracellular matrix accumulation in kidneys of diabetic mice, accompanied with HDAC5, TGF-β1, and α-SMA expression downregulation. These above data suggest that METTL14-regulated PI3K/Akt signaling pathway via PTEN affected HDAC5-mediated EMT of renal tubular cells in diabetic kidney disease.

scholarly journals Interleukin-22 attenuates renal tubular cells inflammation and fibrosis induced by TGF-β1 through Notch1 signaling pathway

Renal Failure ◽  
2020 ◽  
Vol 42 (1) ◽  
pp. 381-390 ◽  
Author(s):  
Rong Tang ◽  
Xiangcheng Xiao ◽  
Yang Lu ◽  
Huihui Li ◽  
Qiaoling Zhou ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Tubular Cells ◽  
Interleukin 22 ◽  
Renal Tubular Cells ◽  
Notch1 Signaling ◽  
Renal Tubular ◽  
Notch1 Signaling Pathway ◽  
Tgf Β1

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 Prostaglandin E1 attenuates high glucose-induced apoptosis in proximal renal tubular cells by inhibiting the JNK/Bim pathway

2019 ◽  
Vol 41 (4) ◽  
pp. 561-571 ◽  
Author(s):  
Yu-han Zhang ◽  
Ya-qin Zhang ◽  
Cong-cong Guo ◽  
Li-kang Wang ◽  
Yu-jiao Cui ◽  
...  
Keyword(s):  
High Glucose ◽  
Prostaglandin E1 ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Induced Apoptosis

ERK and p38 mediate high-glucose-induced hypertrophy and TGF-β expression in renal tubular cells

2004 ◽  
Vol 286 (1) ◽  
pp. F120-F126 ◽  
Author(s):  
Hisayo Fujita ◽  
Sayu Omori ◽  
Kenji Ishikura ◽  
Mariko Hida ◽  
Midori Awazu
Keyword(s):  
High Glucose ◽  
Transforming Growth Factor ◽  
Mek Inhibitor ◽  
Mitogen Activated Protein Kinase ◽  
Leucine Incorporation ◽  
Renal Tubules ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Sb 203580

We investigated the expression of ERK, p38 mitogen-activated protein kinase (p38), and JNK in renal tubules of diabetic rats following 3 wk after streptozotocin injection (DM). Although the expression of ERK was not different between controls and DM, phosphorylated ERK was expressed more intensely in DM. p38 And phosphorylated p38 were detected only in the diabetic kidney and were localized in all tubular segments. JNK and phosphorylated JNK were expressed similarly in controls and DM. Transforming growth factor (TGF)-β was expressed in all tubular segments of DM, coinciding with the localization of p38. In LLC-PK1 cells, phosphorylation of ERK and p38 increased after 24- to 72-h exposure to high glucose (HG). Coincubation with a p38 inhibitor SB-203580 or a MEK inhibitor, PD-98059, suppressed the HG-induced increases in protein content, [3H]leucine incorporation, and the protein-to-DNA ratio. SB-203580 or PD-98059 also abolished the HG-stimulated expression of TGF-β protein. These results demonstrate that ERK and p38 are activated in renal tubular cells of DM and may mediate HG-induced cellular hypertrophy and TGF-β expression.

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