The Protective Roles of Estrogen Receptor <i>β</i> in Renal Calcium Oxalate Crystal Formation <i>via</i> Reducing the Liver Oxalate Biosynthesis and Renal Oxidative Stress-Mediated Cell Injury

Zhu, Wei; Zhao, Zhijian; Chou, Fu-Ju; Zuo, Li; Liu, Tongzu; Bushinsky, David A.; Chang, Chawnshang; Zeng, Guohua; Yeh, Shuyuan

doi:10.1155/2019/5305014

Cited by 31 publications

(30 citation statements)

References 52 publications

(58 reference statements)

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“…NADPH oxidase is confirmed as the main source of free radicals in kidneys, Liang et al found that the activation of androgen receptor (AR) signaling contributed to the upregulation of NADPH oxidase, which increased oxalate biosynthesis and oxidative stress, inducing kidney tubular injury and promoting stone formation 35 . In another study, estrogen/estrogen receptor beta (ERβ) exerted protective effect on renal CaOx crystal formation by inhibiting liver oxalate biosynthesis and reducing the expression of NADPH oxidase subunit 2 (NOX2) 36 . Sun et al reported pretreatment with taurine markedly reduced oxidative stress by promoting SOD2 activity and decreasing MDA concentration, and also suppressed ROS-dependent autophagy through activating Akt/mTOR pathway, thus alleviating crystal-induced oxidative injury in kidney tissues and HK-2 cells 37 .…”

Section: Discussionmentioning

confidence: 99%

Theaflavin protects against oxalate calcium-induced kidney oxidative stress injury via upregulation of SIRT1

Ye¹,

Yang²,

Liu³

et al. 2021

Int. J. Biol. Sci.

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Renal tubular cell injury induced by calcium oxalate (CaOx) is a critical initial stage of kidney stone formation. Theaflavin (TF) has been known for its strong antioxidative capacity; however, the effect and molecular mechanism of TF against oxidative stress and injury caused by CaOx crystal exposure in kidneys remains unknown. To explore the potential function of TF on renal crystal deposition and its underlying mechanisms, experiments were conducted using a CaOx nephrocalcinosis mouse model established by glyoxylate intraperitoneal injection, and HK-2 cells were subjected to calcium oxalate monohydrate (COM) crystals, with or without the treatment of TF. We discovered that TF treatment remarkably protected against CaOx-induced kidney oxidative stress injury and reduced crystal deposition. Additionally, miR-128-3p expression was decreased and negatively correlated with SIRT1 level in mouse CaOx nephrocalcinosis model following TF treatment. Moreover, TF suppressed miR-128-3p expression and further abolished its inhibition on SIRT1 to attenuate oxidative stress in vitro. Mechanistically, TF interacted with miR-128-3p and suppressed its expression. In addition, miR-128-3p inhibited SIRT1 expression by directly binding its 3'-untranslated region (UTR). Furthermore, miR-128-3p activation partially reversed the acceerative effect of TF on SIRT1 expression. Taken together, TF exhibits a strong nephroprotective ability to suppress CaOx-induced kidney damage through the recovery of the antioxidant defense system regulated by miR-128-3p/SIRT1 axis. These findings provide novel insights for the prevention and treatment of renal calculus.

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Section: Discussionmentioning

confidence: 99%

Theaflavin protects against oxalate calcium-induced kidney oxidative stress injury via upregulation of SIRT1

Ye¹,

Yang²,

Liu³

et al. 2021

Int. J. Biol. Sci.

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show abstract

“…Studies have shown that a high concentration of oxalate could lead to renal injury and contribute considerably to the deposition and progression of calcium oxalate crystals [ 3 ]. A large amount of evidence suggests that increased calcium oxalate crystal adherence to and aggregation in renal tubular cells are related to the overproduction of reactive oxygen species (ROS) [ 4 ]. ROS result in serious renal tissue injuries, such as lipid peroxidation of the cellular membranes, presumably through OS [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Calcium-sensing receptor promotes calcium oxalate crystal adhesion and renal injury in Wistar rats by promoting ROS production and subsequent regulation of PS ectropion, OPN, KIM-1, and ERK expression

Chen

Feng

et al. 2021

Renal Failure

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Objectives To explore the mechanism of calcium-sensing receptors (CaSRs) during the development of nephrolithiasis. Materials and methods Wistar rats were treated with ethylene glycol to induce calcium oxalate crystallization, and gadolinium chloride (GdCl 3 , an agonist of CaSR) and NPS 2390 (an antagonist of CaSR) were added. Oxidative stress (OS) and calcium oxalate crystals in the kidney were observed. CaSR expression and the expression of extracellular signal-regulated protein kinase (ERK), OPN, and KIM-1 were determined by western blotting. In addition, renal tubular epithelial cells were isolated from the kidney to observe phosphatidylserine (PS) ectropion using flow cytometric analysis. Various biochemical parameters were assessed in serum and urine at the end of the experiment. Results Calcium oxalate increased OS, crystal adhesion, PS ectropion, and the expression of CaSR and ERK, OPN, and KIM-1 in vivo . In addition, lower levels of urine citrate as well as increased serum creatinine and urea levels were observed after treatment with calcium oxalate ( p < .05). Compared with calcium oxalate treatment alone, the above deleterious changes were further significantly confirmed by GdCl 3 but were reversed by NPS-2390. However, urine calcium excretion was decreased after ethylene glycol treatment but was significantly reduced by NPS 2390 and increased by GdCl 3 ( p < .05). Conclusions The results suggest that CaSR might play significant roles in the induction of nephrolithiasis in rats by regulating reactive oxygen species (ROS) and PS ectropion and the composition of urine, OPN, KIM-1, and ERK expression.

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“…Moreover, many studies also indicated that renal CaOx crystal deposition could be significantly decreased by antioxidant treatment in vivo [7,27,28]. Many other studies found that ROS is a key factor in the formation of CaOx stones by regulating a variety of signaling pathways, including the NF-κB pathway [29][30][31][32]. And Liu et al also found that the interaction between H19 and miR-216b promotes ROS and renal tubular epithelial cell injury in the process of CaOx nephrocalcinosis by HMGB1/TLR4/NF-κB pathway [12].…”

Section: Discussionmentioning

confidence: 99%

miR-155-5p Promotes Oxalate- and Calcium-Induced Kidney Oxidative Stress Injury by Suppressing MGP Expression

Jiang

Luo

et al. 2020

Oxidative Medicine and Cellular Longevity

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Oxalate and calcium are the major risk factors for calcium oxalate (CaOx) stone formation. However, the exact mechanism remains unclear. This study was designed to confirm the potential function of miR-155-5p in the formation of CaOx induced by oxalate and calcium oxalate monohydrate (COM). The HK-2 cells were treated by the different concentrations of oxalate and COM for 48 h. We found that oxalate and COM treatment significantly increased ROS generation, LDH release, cellular MDA levels, and H2O2 concentration in HK-2 cells. The results of qRT-PCR and western blot showed that expression of NOX2 was upregulated, while that of SOD-2 was downregulated following the treatment with oxalate and COM in HK-2 cells. Moreover, the results of miRNA microarray analysis showed that miR-155-5p was significantly upregulated after oxalate and COM treated in HK-2 cells, but miR-155-5p inhibitor treatment significantly decreased ROS generation, LDH release, cellular MDA levels, and H2O2 concentration in HK-2 cells incubated with oxalate and COM. miR-155-5p negatively regulated the expression level of MGP via directly targeting its 3′-UTR, verified by the Dual-Luciferase Reporter System. In vivo, polarized light optical microphotography showed that CaOx crystal significantly increased in the high-dose oxalate and Ca2+ groups compared to the control group. Furthermore, IHC analyses showed strong positive staining intensity for the NOX-2 protein in the high-dose oxalate and Ca2+-treated mouse kidneys, and miR-155-5p overexpression can further enhance its expression. However, the expression of SOD-2 protein was weakly stained. In conclusion, our study indicates that miR-155-5p promotes oxalate- and COM-induced kidney oxidative stress injury by suppressing MGP expression.

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The Protective Roles of Estrogen Receptor β in Renal Calcium Oxalate Crystal Formation via Reducing the Liver Oxalate Biosynthesis and Renal Oxidative Stress-Mediated Cell Injury

Cited by 31 publications

References 52 publications

Theaflavin protects against oxalate calcium-induced kidney oxidative stress injury via upregulation of SIRT1

Theaflavin protects against oxalate calcium-induced kidney oxidative stress injury via upregulation of SIRT1

Calcium-sensing receptor promotes calcium oxalate crystal adhesion and renal injury in Wistar rats by promoting ROS production and subsequent regulation of PS ectropion, OPN, KIM-1, and ERK expression

miR-155-5p Promotes Oxalate- and Calcium-Induced Kidney Oxidative Stress Injury by Suppressing MGP Expression

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