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Start Over Descriptor "kidney endothelial cell" Topic apoptosis
2 results on '"kidney endothelial cell"'

1. High Concentration of C5a-Induced Mitochondria-Dependent Apoptosis in Murine Kidney Endothelial Cells.

Author

Tsai IJ, Lin WC, Yang YH, Tseng YL, Lin YH, Chou CH, and Tsau YK

Subjects
Acetylcysteine pharmacology, Aniline Compounds pharmacology, Animals, Caspases metabolism, Cell Survival drug effects, Cells, Cultured, Complement C5a genetics, Cytochromes c metabolism, Dose-Response Relationship, Drug, Endothelial Cells metabolism, Free Radical Scavengers pharmacology, Humans, Kidney cytology, Mice, Reactive Oxygen Species metabolism, Receptor, Anaphylatoxin C5a antagonists & inhibitors, Receptor, Anaphylatoxin C5a metabolism, Tetrahydronaphthalenes pharmacology, Apoptosis drug effects, Complement C5a pharmacology, Endothelial Cells drug effects, Mitochondria metabolism, Recombinant Proteins pharmacology
Abstract

Patients with a relapse of idiopathic nephrotic syndrome have significantly increased levels of serum complement component 5a (C5a), and proteinuria has been noted in mice treated with C5a via changes in permeability of kidney endothelial cells (KECs) in established animal models. However, the apoptosis of KECs treated with high concentrations of C5a has also been observed. As mitochondrial damage is known to be important in cell apoptosis, the aim of this study was to examine the association between C5a-induced mouse KEC apoptosis and mitochondrial damage. Mouse KECs were isolated and treated with different concentrations of C5a. Cell viability assays showed that a high-concentration mouse recombinant protein C5a (rmC5a) treatment reduced mouse KEC growth. Cell cycle phase analysis, including apoptosis (sub-G1 phase) showed an increased percentage of the subG1 phase with a high-concentration rmC5a treatment. Cytochrome c and caspase 3/9 activities were significantly induced in the mouse KECs after a high-dose rmC5a (50 ng/mL) treatment, and this was rescued by pretreatment with the C5a receptor (C5aR) inhibitor (W-54011) and N-acetylcysteine (NAC). Reactive oxygen species (ROS) formation was detected in C5a-treated mouse KECs; however, W-54011 or NAC pretreatment inhibited high-dose rmC5a-induced ROS formation and also reduced cytochrome c release, apoptotic cell formation, and apoptotic DNA fragmentation. These factors determined the apoptosis of mouse KECs treated with high-dose C5a through C5aR and subsequently led to apoptosis via ROS regeneration and cytochrome c release. The results showed that high concentrations of C5a induced mouse KEC apoptosis via a C5aR/ROS/mitochondria-dependent pathway. These findings may shed light on the potential mechanism of glomerular sclerosis, a process in idiopathic nephrotic syndrome causing renal function impairment.

Published
2019
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2. High Concentration of C5a-Induced Mitochondria-Dependent Apoptosis in Murine Kidney Endothelial Cells

Author

Chia-Hung Chou, Yen-Hung Lin, Yu-Lin Tseng, Yong-Kwei Tsau, Yao-Hsu Yang, Wei-Chou Lin, and I-Jung Tsai

Subjects
0301 basic medicine, Mitochondrion, Kidney, lcsh:Chemistry, Mice, 0302 clinical medicine, lcsh:QH301-705.5, Spectroscopy, Cells, Cultured, kidney endothelial cell, chemistry.chemical_classification, Aniline Compounds, biology, Chemistry, Cytochrome c, Apoptotic DNA fragmentation, apoptosis, Cytochromes c, hemic and immune systems, General Medicine, Free Radical Scavengers, Recombinant Proteins, Computer Science Applications, mitochondria, 030220 oncology & carcinogenesis, Caspases, C5a, Tetrahydronaphthalenes, Cell Survival, Caspase 3, chemical and pharmacologic phenomena, Complement C5a, Catalysis, Article, Cell cycle phase, Inorganic Chemistry, 03 medical and health sciences, Animals, Humans, Viability assay, Physical and Theoretical Chemistry, Molecular Biology, Receptor, Anaphylatoxin C5a, Reactive oxygen species, Dose-Response Relationship, Drug, ROS regeneration, Organic Chemistry, Endothelial Cells, Molecular biology, Acetylcysteine, 030104 developmental biology, lcsh:Biology (General), lcsh:QD1-999, Apoptosis, biology.protein, Reactive Oxygen Species
Abstract

Patients with a relapse of idiopathic nephrotic syndrome have significantly increased levels of serum complement component 5a (C5a), and proteinuria has been noted in mice treated with C5a via changes in permeability of kidney endothelial cells (KECs) in established animal models. However, the apoptosis of KECs treated with high concentrations of C5a has also been observed. As mitochondrial damage is known to be important in cell apoptosis, the aim of this study was to examine the association between C5a-induced mouse KEC apoptosis and mitochondrial damage. Mouse KECs were isolated and treated with different concentrations of C5a. Cell viability assays showed that a high-concentration mouse recombinant protein C5a (rmC5a) treatment reduced mouse KEC growth. Cell cycle phase analysis, including apoptosis (sub-G1 phase) showed an increased percentage of the subG1 phase with a high-concentration rmC5a treatment. Cytochrome c and caspase 3/9 activities were significantly induced in the mouse KECs after a high-dose rmC5a (50 ng/mL) treatment, and this was rescued by pretreatment with the C5a receptor (C5aR) inhibitor (W-54011) and N-acetylcysteine (NAC). Reactive oxygen species (ROS) formation was detected in C5a-treated mouse KECs, however, W-54011 or NAC pretreatment inhibited high-dose rmC5a-induced ROS formation and also reduced cytochrome c release, apoptotic cell formation, and apoptotic DNA fragmentation. These factors determined the apoptosis of mouse KECs treated with high-dose C5a through C5aR and subsequently led to apoptosis via ROS regeneration and cytochrome c release. The results showed that high concentrations of C5a induced mouse KEC apoptosis via a C5aR/ROS/mitochondria-dependent pathway. These findings may shed light on the potential mechanism of glomerular sclerosis, a process in idiopathic nephrotic syndrome causing renal function impairment.

Published
2019

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