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.

Adiponectin attenuates angiotensin II-induced oxidative stress in renal tubular cells through AMPK and cAMP-Epac signal transduction pathways

2013 ◽  
Vol 304 (11) ◽  
pp. F1366-F1374 ◽  
Author(s):  
Fei Fang ◽  
George C. Liu ◽  
Crystal Kim ◽  
Rana Yassa ◽  
Joyce Zhou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Protective Role ◽  
Ang Ii ◽  
Ckd Progression ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Compound C ◽  
Renal Tubular ◽  
Nadph Oxidase Activation

Obesity is a risk factor for chronic kidney disease (CKD) progression. Circulating levels of adiponectin, an adipokine, decrease with obesity and play a protective role in the cardiovascular system. We hypothesized that adiponectin might also protect the kidney. Because activation of the renin-angiotensin system (RAS) is a contributor to CKD progression, we tested our hypothesis by studying the interactions between adiponectin and angiotensin II (ANG II) in renal tubular cells. Primary human renal proximal tubule cells expressed both adiponectin receptor 1 and 2 (adipoR1 and R2). ANG II-induced NADPH oxidase activation and oxidative stress were attenuated by adiponectin and dependent on adipoR1. Activation of AMPK with 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR) mimicked, while inhibition of AMPK with compound C abrogated, the effect of adiponectin on ANG II-induced activation of NADPH oxidase. Similarly, the effect of adiponectin was recapitulated by the stable cAMP analogs 4-chlorophenylthio (pCPT)-cAMP and dibutyryl (db)-cAMP and blocked by the adenylate cyclase inhibitor SQ22536. Adiponectin did not activate PKA in renal tubular cells, and the specific PKA inhibitor myristoylated PKI (14–22) amide failed to block the inhibitory effect of adiponectin on ANG II-induced NADPH oxidase activation. In contrast, the specific Epac activator 8-(4-chlorophenylthio)-2′-O-methyl (8-CPT-2-O-Me)-cAMP blocked ANG II-induced activation of NADPH oxidase, an effect that was reversed by coincubation with the AMPK inhibitor compound C. Finally, adiponectin attenuated ANG II-induced NF-κB activation and fibronectin protein expression. These in vitro findings support the hypothesis that adiponectin may attenuate the deleterious effects of ANG II in the kidney and play a protective role in CKD.

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

Leptin Induces Oxidative Stress Through Activation of NADPH Oxidase in Renal Tubular Cells: Antioxidant Effect of L-Carnitine

2016 ◽  
Vol 117 (10) ◽  
pp. 2281-2288 ◽  
Author(s):  
Antonio J. Blanca ◽  
María V. Ruiz-Armenta ◽  
Sonia Zambrano ◽  
Rocío Salsoso ◽  
José L. Miguel-Carrasco ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Antioxidant Effect ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular

scholarly journals p66Shc mediates high-glucose and angiotensin II-induced oxidative stress renal tubular injury via mitochondrial-dependent apoptotic pathway

2010 ◽  
Vol 299 (5) ◽  
pp. F1014-F1025 ◽  
Author(s):  
Lin Sun ◽  
Li Xiao ◽  
Jing Nie ◽  
Fu-you Liu ◽  
Guang-hui Ling ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cytochrome C ◽  
High Glucose ◽  
Dominant Negative ◽  
Renal Tubules ◽  
Ang Ii ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Pkc Β ◽  
Renal Tubular

p66Shc, a promoter of apoptosis, modulates oxidative stress response and cellular survival, but its role in the progression of diabetic nephropathy is relatively unknown. In this study, mechanisms by which p66Shc modulates high-glucose (HG)- or angiotensin (ANG) II-induced mitochondrial dysfunction were investigated in renal proximal tubular cells (HK-2 cells). Expression of p66Shc and its phosphorylated form (p-p66Shc, serine residue 36) and apoptosis were notably increased in renal tubules of diabetic mice, suggesting an increased reactive oxygen species production. In vitro, HG and ANG II led to an increased expression of total and p-p66Shc in HK-2 cells. These changes were accompanied with increased production of mitochondrial H2O2, reduced mitochondrial membrane potential, increased translocation of mitochondrial cytochrome c from mitochondria into cytosol, upregulation of the expression of caspase-9, and ultimately reduced cell survival. Overexpression of a dominant-negative Ser36 mutant p66Shc (p66ShcS36A) or treatment of p66Shc- or PKC-β-short interfering RNAs partially reversed these changes. Treatment of HK-2 cells with HG and ANG II also increased the protein-protein association between p-p66Shc and Pin1, an isomerase, in the cytosol, and with cytochrome c in the mitochondria. These interactions were partially disrupted with the treatment of PKC-β inhibitor or Pin1-short interfering RNA. These data suggest that p66Shc mediates HG- and ANG II-induced mitochondrial dysfunctions via PKC-β and Pin1-dependent pathways in renal tubular cells.

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 Effects of Hyaluronic Acid on Calcium Oxalate Crystallization, Growth, Aggregation, Adhesion on Renal Tubular Cells, and Invasion Through Extracellular Matrix

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 13-13
Author(s):  
Chanettee Chanthick ◽  
Visith Thongboonkerd
Keyword(s):  
Extracellular Matrix ◽  
Hyaluronic Acid ◽  
Crystal Growth ◽  
Calcium Oxalate ◽  
Kidney Stone ◽  
Stone Formation ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Kidney Stone Formation

Abstract Objectives Hyaluronic acid (HA), a large non-sulfated glycosaminoglycan, is one of the major components of extracellular matrix (ECM) in connective tissues and other organs. Currently, it is widely used as a dietary supplement, especially for treatment or prevention of aging-related disorders. On the other hand, HA has been reported with an increased risk of kidney stone disease, particularly calcium oxalate (CaOx) type, but with unclear mechanisms. We therefore performed systematic analyses for its modulatory effects on CaOx monohydrate (COM) crystal at various steps of kidney stone formation processes. Methods HA at 1, 10, 100, 1000 and 10,000 ng/ml was tested in various assays for COM crystallization, crystal growth, aggregation, crystal-cell adhesion and invasion through ECM. Results COM crystallization and crystal aggregation were not affected by HA at all concentrations. However, HA significantly promoted COM crystal growth and adhesion onto renal tubular cells in a dose-dependent manner. Interestingly, COM crystal invasion through the ECM was dramatically enhanced by HA even at very low concentration (such as 1 ng/ml). Conclusions Our findings provide evidence for promoting effects of HA on COM crystal growth, adhesion on renal tubular cell surface and invasion through the ECM, all of which are the important steps for kidney stone formation. Funding Sources TRF-IRN grant.

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