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137 results on '"Xu, Luwei"'

20. Cystine crystal-induced reactive oxygen species associated with NLRP3 inflammasome activation: implications for the pathogenesis of cystine calculi

Author

Zhang Yifan, Shen Luming, Chen Wei, Xu Luwei, Xu Zheng, and Jia Ruipeng

Subjects
Nephrology, Inflammasomes, Urology, Interleukin-1beta, NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Cystine, Hydrogen Peroxide, RNA, Messenger, RNA, Small Interfering, Reactive Oxygen Species, Calculi, Rats
Abstract

To investigate whether cystine crystal-induced production of reactive oxygen species (ROS) and activation of NLRP3 inflammasome contribute to cystine calculi formation.Slc7a9-knockout rats were created as cystine calculi animal models. Kidney histological examination using TEM and immunohistochemistry were performed. The protein expression of NLRP3 and IL-1β and the concentrations of oxidative stress markers such as ROS, MDA and H2O2 in kidney tissues were estimated. In parallel, HK-2 human renal proximal tubule cells were exposed to cystine crystals and NAC treatment. The protein and mRNA expression levels of NLRP3 were evaluated. Finally, cell apoptosis and cystine crystal adherence were also assessed.Activation of the NLRP3 inflammasome and marked elevations in MDA, H2O2 and ROS levels were observed both in vivo and in vitro. In particular, the protein and mRNA expression of NLRP3 was significantly increased by cystine crystals, but could be restored by an inhibitor of ROS. In addition, cell apoptosis and cystine crystal adherence were promoted by the NLRP3 inflammasome. The expression of CD44, OPN and HA in HK-2 cells was markedly increased by cystine crystals, but could be decreased by NLRP3 siRNA treatment.Notably, we found that the activation of NLRP3 by cystine crystal-induced ROS production was of major importance in the pathogenesis of cystine calculi formation.

Published
2022

23. Additional file 1 of Comprehensive insight into endothelial progenitor cell-derived extracellular vesicles as a promising candidate for disease treatment

Author

Chen, Ke, Li, Yang, Xu, Luwei, Qian, Yiguan, Liu, Ning, Zhou, Changcheng, Liu, Jingyu, Zhou, Liuhua, Xu, Zheng, Jia, Ruipeng, and Ge, Yu-Zheng

Subjects
embryonic structures, cardiovascular system, circulatory and respiratory physiology
Abstract

Additional file1: Table S1. The beneficial effects of EPC-EVs on various diseases.

Published
2022
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25. Tumor Cell-Derived Exosomal circ-PRKCI Promotes Proliferation of Renal Cell Carcinoma via Regulating miR-545-3p/CCND1 Axis.

Author

Qian, Yiguan, Li, Yang, Xu, Luwei, Chen, Ke, Liu, Ning, Yang, Xiaobing, Lv, Qian, Li, Rongfei, Zhou, Changcheng, Xu, Zheng, Jia, Ruipeng, and Ge, Yu-Zheng

Subjects
RENAL cell carcinoma, IN vitro studies, CIRCULAR RNA, DISEASE progression, EXOSOMES, ANIMAL experimentation, CANCER invasiveness, METASTASIS, ORGANIC compounds, GENE expression, CELL motility, CELL proliferation, EPITHELIAL cells, CELL lines, TUMOR markers
Abstract

Simple Summary: The morbidity and mortality of renal cell carcinoma (RCC) remain high, and there is an urgent need to explore the reliable biomarker and molecular mechanism of RCC. Circ-PRKCI is a novel circRNA discovered in recent years, and has been confirmed to participate in tumor progression by acting as an miRNA sponge. However, the role of circ-PRKCI in RCC remains unclear. Here, with the aid of an online bioinformatics database and luciferase reporter assays, we found that circ-PRKCI could bind to miR-545-3p, while CCND1 served as a target of miR-545-3p. Caki-1-derived exosomes could thus inhibit miR-545-3p expression via the upregulation of circ-PRKCI. Through a series of functional experiments, we confirmed that Caki-1-derived exosomal circ-PRKCI promoted RCC proliferation by regulating the miR-545-3p/CCND1 axis. Our study will provide new insights for RCC clinical treatment. Renal cell carcinoma (RCC) originates from the epithelial cells of the renal tubules and has a high degree of malignancy and heterogeneity. Recent studies have found that exosomes regulate intercellular communication via transferring various bioactive molecules, such as circular RNAs (circRNAs), which are critical for cancer progression. However, the role of tumor cell-derived exosomal circRNAs in RCC remains unclear. In this study, we reported the high expression of circ-PRKCI in RCC tissues and serum exosomes. We also found that circ-PRKCI could be transferred exosomally from highly malignant RCC cells to relatively less malignant RCC cells. Tumor cell-derived exosomal circ-PRKCI promoted the proliferation, migration, and invasion of RCC cells, while inhibiting their apoptosis. Mechanistically, we found that circ-PRKCI promoted the proliferation of RCC via the miR-545-3p/CCND1 signaling pathway. Our study is the first to report the potential mechanisms of tumor cell-derived exosomal circ-PRKCI in RCC. In conclusion, this study will provide a new understanding about the molecular mechanisms of RCC progression. [ABSTRACT FROM AUTHOR]

Published
2023
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33. Ceftriaxone Calcium Crystals Induce Acute Kidney Injury by NLRP3-Mediated Inflammation and Oxidative Stress Injury

Author

Jia Ruipeng, Xu Luwei, Xu Zheng, Ge Yuzheng, Zhang Yifan, Zhou Liuhua, and Ning Benxiang

Subjects
0301 basic medicine, Aging, medicine.medical_specialty, Article Subject, Inflammasomes, 030232 urology & nephrology, chemistry.chemical_element, Calcium, medicine.disease_cause, Biochemistry, Cell Line, Kidney Tubules, Proximal, Rats, Sprague-Dawley, 03 medical and health sciences, 0302 clinical medicine, Urolithiasis, Internal medicine, NLR Family, Pyrin Domain-Containing 3 Protein, medicine, Animals, Humans, Blood urea nitrogen, Calcium metabolism, Kidney, QH573-671, business.industry, Ceftriaxone, Acute kidney injury, Cell Biology, General Medicine, Acute Kidney Injury, medicine.disease, Rats, Oxidative Stress, 030104 developmental biology, medicine.anatomical_structure, Endocrinology, chemistry, Creatinine, Kidney stones, business, Reactive Oxygen Species, Cytology, Oxidative stress, medicine.drug, Research Article
Abstract

Objective. To investigate the role of inflammatory reactions and oxidative stress injury in the mechanisms of ceftriaxone calcium crystal-induced acute kidney injury (AKI) both in vivo and in vitro. Methods. Male Sprague Dawley rats were randomly divided into five groups of ten each according to different concentrations of ceftriaxone and calcium. Based on the levels of serum creatinine (Scr) and blood urea nitrogen (BUN), the AKI group was chosen for the subsequent experiments. Kidney histological examination and immunohistochemistry were performed. The expression of NLRP3 and IL-1β protein and the concentrations of oxidative stress markers such as ROS, MDA, and H2O2 in kidney tissues were estimated. In parallel, HK-2 human renal proximal tubule cells were exposed to ceftriaxone calcium crystals. The mRNA expression levels of NLRP3 and IL-1β and the concentrations of oxidative stress markers were evaluated. Finally, cell viability and rat survival were also assessed. Results. The results showed that significantly increased Scr and BUN levels, consistent with morphological changes and kidney stones, were found in the rats that received the highest concentration of ceftriaxone (1000 mg/kg) combined with calcium (800 mg/kg). The activation of the NLRP3 inflammasome axis and the marked elevation of MDA, H2O2, and ROS levels were observed both in vivo and in vitro. High expression of Nrf2, HO-1, and NQO1 was also documented. In addition, cell apoptosis and rat mortality were promoted by ceftriaxone calcium crystals. Conclusions. Notably, we found that ceftriaxone-induced urolithiasis was associated with a high risk of AKI and NLRP3-mediated inflammasome and oxidative stress injury were of major importance in the pathogenesis.

Published
2020

34. Kidney extracellular matrix hydrogel enhances therapeutic potential of adipose-derived mesenchymal stem cells for renal ischemia reperfusion injury

Author

Zhou, Changcheng, primary, Zhou, Liuhua, additional, Liu, Jingyu, additional, Xu, Luwei, additional, Xu, Zheng, additional, Chen, Zaozao, additional, Ge, Yuzheng, additional, Zhao, Feng, additional, Wu, Ran, additional, Wang, Xinning, additional, Jiang, Nan, additional, Mao, Liang, additional, and Jia, Ruipeng, additional

Published
2020
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42. Protective effect of salvianolic acid B against oxidative injury associated with cystine stone formation

Author

Jia Ruipeng, Zhou Liuhua, Xu Luwei, Ge Yuzheng, Zhang Yifan, and Liang Kai

Subjects
Male, medicine.medical_specialty, Antioxidant, Urology, medicine.medical_treatment, 030232 urology & nephrology, Cystine, Oxidative phosphorylation, medicine.disease_cause, Superoxide dismutase, 03 medical and health sciences, chemistry.chemical_compound, Kidney Calculi, Mice, 0302 clinical medicine, Internal medicine, medicine, Animals, Humans, Viability assay, Cells, Cultured, Benzofurans, chemistry.chemical_classification, Mice, Knockout, biology, Chemistry, Glutathione peroxidase, Malondialdehyde, Oxidative Stress, Endocrinology, biology.protein, Oxidative stress
Abstract

The aim of this study was to investigate the role of oxidative stress in cystine crystal formation and whether salvianolic acid B, a natural antioxidant, could prevent cystine-mediated oxidative injury in vivo and in vitro. The levels of oxidative stress and antioxidase activity in cystine stone patients were assessed. Then, the oxidative stress exerted by cystine on human kidney-2 (HK-2) cell viability and biochemical parameters including antioxidase activity and antioxidant protein expression were evaluated, and the protective action of salvianolic acid B was also examined. Finally, salvianolic acid B was tested to determine whether it could prevent or reduce renal crystal formation in Slc7a9 knockout mice. The activity levels of superoxide dismutase (SOD) and glutathione peroxidase (GPx) were decreased, and the amount of malondialdehyde (MDA) was increased in patients with cystine stones compared with people without cystine stones (p

Published
2018

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