Effects of cadmium chloride on the functional state of human intestinal cells

Русанов, А. Л.; Smirnova, Angela V.; Поромов, А. А.; Fomicheva, K. A.; Лузгина, Н. Г.; Majouga, Alexander G.

doi:10.1016/j.tiv.2015.03.018

Cited by 28 publications

(10 citation statements)

References 27 publications

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“…Moreover, accordingly to previously reported data in other cell lines [80,81,82,83], our results revealed that 10 μM CdCl 2 induced an extensive alteration of the localization pattern of ZO-1 TJ protein as well as the cytoskeletal F-actin and vimentin proteins in RBE4 endothelial cells, indicating that TJs and associated proteins are primary targets of Cd. The choice to examine the Cd effects on ZO-1 depended on the fact that RBE4 cells are induced to synthesize and correctly localize occludin [84] and claudin-5 at the cell periphery and at the cell–cell junctions, only if endothelial cells are cocultured with neurons [79,85].…”

Section: Discussionsupporting

confidence: 91%

Effects of Cadmium on ZO-1 Tight Junction Integrity of the Blood Brain Barrier

Branca

Maresca

Morucci

et al. 2019

IJMS

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Cadmium (Cd) is a highly toxic environmental pollutant released from the smelting and refining of metals and cigarette smoking. Oral exposure to cadmium may result in adverse effects on a number of tissues, including the central nervous system (CNS). In fact, its toxicity has been related to neurological disorders, as well as neurodegenerative diseases such as Alzheimer’s and Parkinson’s diseases. Under normal conditions, Cd barely reaches the brain in adults because of the presence of the blood–brain barrier (BBB); however, it has been demonstrated that Cd-dependent BBB alteration contributes to pathogenesis of neurodegeneration. However, the mechanism underlying Cd-dependent BBB alteration remain obscure. Here, we investigated the signaling pathway of Cd-induced tight junction (TJ), F-actin, and vimentin protein disassembly in a rat brain endothelial cell line (RBE4). RBE4 cells treated with 10 μM cadmium chloride (CdCl2) showed a dose- and time-dependent significant increase in reactive oxygen species (ROS) production. This phenomenon was coincident with the alteration of the TJ zonula occludens-1 (ZO-1), F-actin, and vimentin proteins. The Cd-dependent ROS increase elicited the upregulation of GRP78 expression levels, a chaperone involved in endoplasmic reticulum (ER) stress that induces caspase-3 activation. Further signal profiling by the pannexin-1 (PANX1) specific inhibitor 10Panx revealed a PANX1-independent increase in ATP spillage in Cd-treated endothelial cells. Our results point out that a ROS-dependent ER stress-mediated signaling pathway involving caspase-3 activation and ATP release is behind the BBB morphological alterations induced by Cd.

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Section: Discussionsupporting

confidence: 91%

Effects of Cadmium on ZO-1 Tight Junction Integrity of the Blood Brain Barrier

Branca

Maresca

Morucci

et al. 2019

IJMS

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“…Many studies demonstrated the ability of Cd2? to modulate the activity of cellular enzymes, to suppress mitochondrial functions, to initiate oxidative stress, and to disrupt calcium homeostasis (Tchounwou et al 2012;Rusanov et al 2015). Moreover, in our previous study we demonstrated the ability of this heavy metal to modulate innate immune responses in IPEC-J2 cells as a function of both time and concentration (Razzuoli et al 2018).…”

Section: Introductionmentioning

confidence: 85%

Characterization of MDCK cells and evaluation of their ability to respond to infectious and non-infectious stressors

et al. 2019

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The Madin-Darby Canine Kidney (MDCK) cell line is widely used as epithelial cell model in studies ranging from viral infection to environmental pollutants, and vaccines production. However, little is known about basal expression of genes involved in innate immunity, and the ability to respond to infectious and non-infectious stressors. Therefore, the aims of our study were to evaluate the basal level of expression of pivotal genes in the innate immune response and cell cycle regulation, as well as to evaluate the ability of this cell line to respond to infectious or non-infectious stressors. As surmised in our working hypothesis, we demonstrated the constitutive expression of genes involved in the innate immune response and cell defense alike, including TLRs, Interleukins, Myd88, p65/NF-kB and p53. Moreover, we described the ability of this cell line to respond to LPS and cadmium (Cd2?) in terms of gene expression and cytokine release. These data confirm the possibility of using this cell line as a model in studies of host/pathogen interaction and response to non-infectious stressors.

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“…HeLa cells obtained from ATCC were cultured in RPMI or DMEM media with the addition of 10% fetal bovine serum (FBS) (Gibco). When they reached 85% of confluence, the cells were subjected to serum-free media containing the following treatments: 0, 5, 50, and 100 μM Cd during different times, the selected doses were previously described by our working group (Cuello-Carrión et al 2015) and coincided with the doses used in other recent publications (Odewumi et al 2015;Panjehpour et al 2010;Rusanov et al 2015). Cd was added to the culture media from a stock solution of 1 mM CdCl 2 .…”

Section: Cell Lines and Treatmentmentioning

confidence: 99%

Recombinant heat shock protein 27 (HSP27/HSPB1) protects against cadmium-induced oxidative stress and toxicity in human cervical cancer cells

Alvarez-Olmedo

Biaggio

Koumbadinga

et al. 2017

Cell Stress and Chaperones

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Cadmium (Cd) is a carcinogen with several well-described toxicological effects in humans, but its molecular mechanisms are still not fully understood. Overexpression of heat shock protein 27 (HSP27/HSPB1)-a multifunctional protein chaperone-has been shown to protect cells from oxidative damage and apoptosis triggered by Cd exposure. The aims of this work were to investigate the potential use of extracellular recombinant HSP27 to prevent/counteract Cd-induced cellular toxicity and to evaluate if peroxynitrite was involved in the development of Cd-induced toxicity. Here, we report that the harmful effects of Cd correlated with changes in oxidative stress markers: upregulation of reactive oxygen species, reduction in nitric oxide (NO) bioavailability, increment in lipid peroxidation, peroxynitrite (PN), and protein nitration; intracellular HSP27 was reduced. Treatments with Cd (100 μM) for 24 h or with the peroxynitrite donor, SIN-1, decreased HSP27 levels (~50%), suggesting that PN formation is responsible for the reduction of HSP27. Pre-treatments of the cells either with Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME) (a pharmacological inhibitor of NO synthase) or with recombinant HSP27 (rHSP27) attenuated the disruption of the cellular metabolism induced by Cd, increasing in a 55 and 52%, respectively, the cell viability measured by CCK-8. Cd induced necrotic cell death pathways, although apoptosis was also activated; pre-treatment with L-NAME or rHSP27 mitigated cell death. Our findings show for the first time a direct relationship between Cd-induced toxicity and PN production and a role for rHSP27 as a potential therapeutic agent that may counteract Cd toxicity.

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Effects of cadmium chloride on the functional state of human intestinal cells

Cited by 28 publications

References 27 publications

Effects of Cadmium on ZO-1 Tight Junction Integrity of the Blood Brain Barrier

Effects of Cadmium on ZO-1 Tight Junction Integrity of the Blood Brain Barrier

Characterization of MDCK cells and evaluation of their ability to respond to infectious and non-infectious stressors

Recombinant heat shock protein 27 (HSP27/HSPB1) protects against cadmium-induced oxidative stress and toxicity in human cervical cancer cells

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