scholarly journals Growth Factors and Oxidative Stress Act Oppositely on Chaperone‐Mediated Autophagy (CMA) in Renal Tubular Cells: Differences in FoxO1 abundance

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Harold A. Franch ◽  
Nikia S. Brown ◽  
Wen Shen
Keyword(s):  
Oxidative Stress ◽  
Growth Factors ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Chaperone Mediated Autophagy ◽  
And Oxidative Stress

scholarly journals BMP7 reduces inflammation and oxidative stress in diabetic tubulopathy

2014 ◽  
Vol 128 (4) ◽  
pp. 269-280 ◽  
Author(s):  
Rui Xi Li ◽  
Wai Han Yiu ◽  
Hao Jia Wu ◽  
Dickson W. L. Wong ◽  
Loretta Y. Y. Chan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Responses ◽  
Advanced Glycation ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Glycation End Products ◽  
Renal Tubular ◽  
Diabetic Tubulopathy ◽  
Oxidative Stress Responses ◽  
And Oxidative Stress

BMP7 ameliorates diabetic tubulopathy by suppressing inflammatory and oxidative stress responses both in cultured renal tubular cells exposed to advanced glycation end-products and in diabetic db/db mice.

scholarly journals Losartan Ameliorates Calcium Oxalate-Induced Elevation of Stone-Related Proteins in Renal Tubular Cells by Inhibiting NADPH Oxidase and Oxidative Stress

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Baolong Qin ◽  
Qing Wang ◽  
Yuchao Lu ◽  
Cong Li ◽  
Henglong Hu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Calcium Oxalate ◽  
Stone Formation ◽  
Ang Ii ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Related Proteins ◽  
And Oxidative Stress

Calcium oxalate (CaOx) is the most common type of urinary stone. Increase of ROS and NADPH oxidase gives rise to inflammation and injury of renal tubular cells, which promotes CaOx stone formation. Recent studies have revealed that the renin-angiotensin system might play a role in kidney crystallization and ROS production. Here, we investigated the involvement of Ang II/AT1R and losartan in CaOx stone formation. NRK-52E cells were incubated with CaOx crystals, and glyoxylic acid-induced hyperoxaluric rats were treated with losartan. Oxidative stress statuses were evaluated by detection of ROS, oxidative products (8-OHdG and MDA), and antioxidant enzymes (SOD and CAT). Expression of NADPH oxidase subunits (Nox2 and Nox4), NF-κB pathway subunits (p50 and p65), and stone-related proteins such as OPN, CD44, and MCP-1 was determined by Western blotting. The results revealed upregulation of Ang II/AT1R by CaOx treatment. CaOx-induced ROS and stone-related protein upregulation were mediated by the Ang II/AT1R signaling pathway. Losartan ameliorated renal tubular cell expression of stone-related proteins and renal crystallization by inhibiting NADPH oxidase and oxidative stress. We conclude that losartan might be a promising preventive and therapeutic candidate for hyperoxaluria nephrolithiasis.

scholarly journals Vitamin C attenuates the toxic effect of aristolochic acid on renal tubular cells via decreasing oxidative stress-mediated cell death pathways

2015 ◽  
Vol 12 (4) ◽  
pp. 6086-6092 ◽  
Author(s):  
TSAI-KUN WU ◽  
CHYOU-WEI WEI ◽  
YING-RU PAN ◽  
SHUR-HUEIH CHERNG ◽  
WEI-JUNG CHANG ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Vitamin C ◽  
Toxic Effect ◽  
Aristolochic Acid ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Cell Death Pathways ◽  
Renal Tubular

Reduction of Oxidative Stress in Cultured Renal Tubular Cells and Preventive Effects on Renal Stone Formation by the Bioflavonoid Quercetin

2008 ◽  
Vol 179 (4) ◽  
pp. 1620-1626 ◽  
Author(s):  
Hyoung Keun Park ◽  
Byong Chang Jeong ◽  
Mi-Kyung Sung ◽  
Mi-Young Park ◽  
Eun Young Choi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renal Stone ◽  
Stone Formation ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Preventive Effects

Examination of the anti-oxidative effect in renal tubular cells and apoptosis by oxidative stress

2005 ◽  
Vol 33 (4) ◽  
pp. 261-266 ◽  
Author(s):  
Yasunori Itoh ◽  
Takahiro Yasui ◽  
Atsushi Okada ◽  
Keiichi Tozawa ◽  
Yutaro Hayashi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Oxidative Effect

scholarly journals Nox4 has a crucial role in uric acid-induced oxidative stress and apoptosis in renal tubular cells

2016 ◽  
Vol 13 (5) ◽  
pp. 4343-4348 ◽  
Author(s):  
Zhuohang Li ◽  
Yiyu Sheng ◽  
Cheng Liu ◽  
Kuiqing Li ◽  
Xin Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Crucial Role ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular

The Role of Growth Factors on Renal Tubular Cells Submitted to Hypoxia and Deprived of Glucose

Renal Failure ◽  
2003 ◽  
Vol 25 (3) ◽  
pp. 341-353 ◽  
Author(s):  
Marcelino de Souza Durão ◽  
Clara Versolato Razvickas ◽  
Elsa Alídia Petry Gonçalves ◽  
Iria Ruriko Okano R.N. ◽  
Simone Mafalda Rodrigues Camargo ◽  
...  
Keyword(s):  
Growth Factors ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular

scholarly journals Nephroprotective Effects of N-Acetylcysteine Amide against Contrast-Induced Nephropathy through Upregulating Thioredoxin-1, Inhibiting ASK1/p38MAPK Pathway, and Suppressing Oxidative Stress and Apoptosis in Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Xuezhong Gong ◽  
Yiru Duan ◽  
Junli Zheng ◽  
Yiquan Wang ◽  
Guohua Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
P38 Mapk ◽  
Mapk Pathway ◽  
Contrast Induced Nephropathy ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
P38 Mapk Pathway ◽  
Thioredoxin 1 ◽  
Renal Tubular

Contrast-induced nephropathy (CIN) is a leading cause of hospital-acquired acute kidney injury (AKI) due to apoptosis induced in renal tubular cells. Our previous study demonstrated the novel N-acetylcysteine amide (NACA); the amide form of N-acetyl cysteine (NAC) prevented renal tubular cells from contrast-induced apoptosis through inhibiting p38 MAPK pathway in vitro. In the present study, we aimed to compare the efficacies of NACA and NAC in preventing CIN in a well-established rat model and investigate whether thioredoxin-1 (Trx1) and apoptosis signal-regulating kinase 1 (ASK1) act as the potential activator for p38 MAPK. NACA significantly attenuated elevations of serum creatinine, blood urea nitrogen, and biomarkers of AKI. At equimolar concentration, NACA was more effective than NAC in reducing histological changes of renal tubular injuries. NACA attenuated activation of p38 MAPK signal, reduced oxidative stress, and diminished apoptosis. Furthermore, we demonstrated that contrast exposure resulted in Trx1 downregulation and increased ASK1/p38 MAPK phosphorylation, which could be reversed by NACA and NAC. To our knowledge, this is the first report that Trx1 and ASK1 are involved in CIN. Our study highlights a renal protective role of NACA against CIN through modulating Trx1 and ASK1/p38 MAPK pathway to result in the inhibition of apoptosis among renal cells.

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