ArticleInternational journal of molecular medicine2016
NF-κB signaling maintains the survival of cadmium-exposed human renal glomerular endothelial cells.
Article in International journal of molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 45 citations in OpenAlex.
- Ameliorative Effects of Zn and Se Supplementation on Heavy Metal Mixture Burden via Increased Renal Metal Excretion and Restoration of Redoxo-Inflammatory Alterations.Biological trace element research · 2024Article
- Review
- Cadmium exposure enhances VE-cadherin expression in endothelial cells via suppression of ROCK signaling.Experimental and therapeutic medicine · 2022Article
- Immunohistochemical, histopathological, and biochemical studies of the NF-ҡB P65 marker in rat ovaries experimentally intoxicated by cadmium and the protective effect of the purslane plant extract.Environmental science and pollution research international · 2021Article
- Manganese exposure induces permeability in renal glomerular endothelial cells via the Smad2/3-Snail-VE-cadherin axis.Toxicology research · 2020Article
- Cadmium regulates von Willebrand factor and occludin expression in glomerular endothelial cells of mice in a TNF-α-dependent manner.Renal failure · 2019Article
- Pathophysiology of aged lymphatic vessels.Aging · 2019Article
- Polyubiquitination of p62/SQSTM1 is a prerequisite for Fas/CD95 aggregation to promote caspase-dependent apoptosis in cadmium-exposed mouse monocyte RAW264.7 cells.Scientific reports · 2019Article
- Rosmarinic Acid Attenuates Cadmium-Induced Nephrotoxicity via Inhibition of Oxidative Stress, Apoptosis, Inflammation and Fibrosis.International journal of molecular sciences · 2019Article
- Dose-Dependent Acute Circulatory Fates Elicited by Cadmium Are Mediated by Differential Engagements of Cardiovascular Regulatory Mechanisms in Brain.Frontiers in physiology · 2019Article
- Impairment of Mitochondrial-Nuclear Cross Talk in Lymphocytes Exposed to Landfill Leachate.Environmental health insights · 2019Article
- Low-intensity pulsed ultrasound in combination with SonoVue induces cytotoxicity of human renal glomerular endothelial cells via repression of the ERK1/2 signaling pathway.Renal failure · 2018Article
- Endoglin-targeted contrast-enhanced ultrasound imaging in hepatoblastoma xenografts.Oncology letters · 2018Article
- Modeling cadmium-induced endothelial toxicity using human pluripotent stem cell-derived endothelial cells.Scientific reports · 2017Article
- Dose dependent effects of cadmium on tumor angiogenesis.Oncotarget · 2017Review
- Low Dose Cadmium Inhibits Proliferation of Human Renal Mesangial Cells via Activation of the JNK Pathway.International journal of environmental research and public health · 2016Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The kidney is one of the primary organs targeted by cadmium (Cd), a widely distributed environmental pollutant. The glomerular endothelium is the major component of the glomerular filtration barrier. However, the effects of Cd on glomerular endothelial cells remain largely unknown. For this purpose, we aimed to determine the effects of low dose Cd on the survival of human renal glomerular endothelial cells (HRGECs). Cultured HRGECs were exposed to 4 µM cadmium chloride (CdCl2) and examined at different time-points. We found that Cd activates the nuclear factor-κB (NF-κB) pathway without inducing the apoptosis of HRGECs. Pre-treating the cells with pyrrolidine dithiocarbamate (PDTC), a potent NF-κB inhibitor, prior to Cd exposure triggered extensive cell death (73.5%). In addition, Cd activates the c-Jun N-terminal kinase (JNK) pathway, and inhibition of the NF-κB pathway significantly elevates Cd-induced JNK phosphorylation in HRGECs (p<0.01). The combination treatment of PDTC and SP600125, a JNK pathway inhibitor, increased the survival of Cd-stimulated HRGECs compared with those cells treated with PDTC alone (p<0.05). Taken together, these findings demonstrate that the NF-κB pathway plays an essential role in maintaining the survival of Cd-exposed HRGECs.
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