Cadmium-induced ceramide formation triggers calpain-dependent apoptosis in cultured kidney proximal tubule cells

Lee, Wing-Kee; Torchalski, Blazej; Thévenod, Frank

doi:10.1152/ajpcell.00197.2007

Cited by 59 publications

(32 citation statements)

References 70 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…has been previously shown to interact with lipids similarly to Ca 2? (Girault et al 1998) and both ions contributed to the externalization of PS in other cell types, inducing apoptosis (Watjen et al 2002;Coonse et al 2007;Lee et al 2007;Sarang et al 2007). In contrast to our Hg 2?…”

Section: Assessment Of Metal Binding Affinity To Liposomescontrasting

confidence: 75%

Hg2+ and Cd2+ interact differently with biomimetic erythrocyte membranes

Gailer

Prenner

2008

Biometals

View full text Add to dashboard Cite

In order to characterize the potentially deleterious effects of toxic Hg(2+) and Cd(2+) on lipid membranes, we have studied their binding to liposomes whose composition mimicked erythrocyte membranes. Fluorescence spectroscopy utilizing the concentration dependent quenching of Phen Green SK by Hg(2+) and Cd(2+) was found to be a sensitive tool to probe these interactions at metal concentrations < or =1 microM. We have systematically developed a metal binding affinity assay to screen for the interactions of Hg(2+) or Cd(2+) with certain lipid classes. A biomimetic liposome system was developed that contained four major lipid classes of erythrocyte membranes (zwitterionic lipids: phosphatidylcholine and phosphatidylethanolamine; negatively charged: phosphatidylserine and neutral: cholesterol). In contrast to Hg(2+), which preferentially bound to the negatively charged phosphatidylserine compared to the zwitterionic components, Cd(2+) bound stronger to the two zwitterionic lipids. Thus, the observed distinct differences in the binding affinity of Hg(2+) and Cd(2+) for certain lipid classes together with their known effects on membrane properties represent an important first step toward a better understanding the role of these interactions in the chronic toxicity of these metals.

show abstract

Section: Assessment Of Metal Binding Affinity To Liposomescontrasting

confidence: 75%

Hg2+ and Cd2+ interact differently with biomimetic erythrocyte membranes

Gailer

Prenner

2008

Biometals

View full text Add to dashboard Cite

show abstract

“…-dependent cysteine protease. The over-activation of calpain is believed to play significant roles in apoptosis and to be connected to a number of disease, including neurodegenerative diseases, RA and cerebral ischemia [31][32][33][34][35][36]. In addition, increased calpain activity can directly cleave calcineurin, resulting in calcineurin phosphatase over-activation, which could initiate a caspase cascade and ultimately lead to cell apoptosis [35].…”

Section: Discussionmentioning

confidence: 99%

Blockade of acid-sensing ion channels protects articular chondrocytes from acid-induced apoptotic injury

Chen

Yuan

et al. 2012

Inflamm. Res.

View full text Add to dashboard Cite

show abstract

“…2, ceramide is known to function as a second messenger in cadmium-induced renal tubule epithelial cell apoptosis via the calpain-caspases pathway. 32,[38][39][40] Exogenous N-hexanoyl-D-erythro-sphingosine (C 6 -ceramide) administration increases cytosolic calcium levels and activates calpains and caspase-3 in rat kidney proximal tubule WKPT-0293 C1.2. cells.…”

Section: Calcium Release From the Ermentioning

confidence: 99%

“…cells. 39) Moreover, the inhibition of de novo ceramide synthesis using a ceramide synthase inhibitor abolishes calpain activation and apoptotic cell death that is caused by acute cadmium exposure in the cells. 38,39) Together, these findings demonstrate that cadmium can also cause an increase in cytosolic calcium levels, which may activate calpain and caspases through an increase in ceramide formation (Fig.…”

Section: Calcium Release From the Ermentioning

confidence: 99%

Cadmium Renal Toxicity <i>via</i> Apoptotic Pathways

Fujiwara

Lee

Tokumoto

et al. 2012

Biological & Pharmaceutical Bulletin

103

View full text Add to dashboard Cite

Cadmium is a nonessential heavy metal and ubiquitous potential environmental pollutant. Although the kidney proximal tubule is an important target for cadmium, the underlying cellular mechanisms of cadmium-induced renal toxicity remain elusive. Numerous studies have demonstrated that cadmium induces apoptotic cell death in various cell types via several apoptotic pathways, including mitochondria-mediated apoptotic cell death. In the epithelial cells of renal proximal tubules, cadmium can also induce apoptotic cell death in vivo and in vitro, which suggests that cell death of the epithelial cells through the apoptotic pathways is one of the key events in cadmium-induced renal toxicity. In this review, based upon the major findings of previous reports related to cadmium and apoptotic cell death, especially in the kidney and kidney proximal tubular cells, we present evidence for the current mechanisms of cadmium-induced renal toxicity via apoptotic cell death.

show abstract

Cadmium-induced ceramide formation triggers calpain-dependent apoptosis in cultured kidney proximal tubule cells

Abstract: Lee W-K, Torchalski B, Thévenod F. Cadmium-induced ceramide formation triggers calpain-dependent apoptosis in cultured kidney proximal tubule cells.

Cited by 59 publications

References 70 publications

Hg2+ and Cd2+ interact differently with biomimetic erythrocyte membranes

Hg2+ and Cd2+ interact differently with biomimetic erythrocyte membranes

Blockade of acid-sensing ion channels protects articular chondrocytes from acid-induced apoptotic injury

Cadmium Renal Toxicity <i>via</i> Apoptotic Pathways

Contact Info

Product

Resources

About