ArticleJournal of cellular and molecular medicine2010
The contact allergen nickel sensitizes primary human endothelial cells and keratinocytes to TRAIL-mediated apoptosis.
Article in Journal of cellular and molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Recent advances in understanding and managing contact dermatitis.F1000Research · 2018Review
- Arginase1 Deficiency in Monocytes/Macrophages Upregulates Inducible Nitric Oxide Synthase To Promote Cutaneous Contact Hypersensitivity.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Immunoproteomic identification and characterization of NiCell death & disease · 2017Article
- Lipopolysaccharide pretreatment inhibits LPS-induced human umbilical cord mesenchymal stem cell apoptosis via upregulating the expression of cellular FLICE-inhibitory protein.Molecular medicine reports · 2015Article
- Carbon nanotubes induce apoptosis resistance of human lung epithelial cells through FLICE-inhibitory protein.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
- Adaptation in the innate immune system and heterologous innate immunity.Cellular and molecular life sciences : CMLS · 2014Review
- Epidermal RelA specifically restricts contact allergen-induced inflammation and apoptosis in skin.The Journal of investigative dermatology · 2014Article
- Allergic contact dermatitis in psoriasis patients: typical, delayed, and non-interacting.PloS one · 2014Article
- FasL and TRAIL signaling in the skin during cutaneous leishmaniasis - implications for tissue immunopathology and infectious control.Frontiers in immunology · 2012Article
- Nickel allergies: paying the Toll for innate immunity.Journal of molecular medicine (Berlin, Germany) · 2011Review
- Animal models for nickel allergy.Nature nanotechnology · 2011Article
- cIAPs block Ripoptosome formation, a RIP1/caspase-8 containing intracellular cell death complex differentially regulated by cFLIP isoforms.Molecular cell · 2011Article
- Cellular FLICE-inhibitory protein (cFLIP) isoforms block CD95- and TRAIL death receptor-induced gene induction irrespective of processing of caspase-8 or cFLIP in the death-inducing signaling complex.The Journal of biological chemistry · 2011Article
- FOXO3 modulates endothelial gene expression and function by classical and alternative mechanisms.The Journal of biological chemistry · 2010Article
- Cellular IAPs inhibit a cryptic CD95-induced cell death by limiting RIP1 kinase recruitment.The Journal of cell biology · 2009Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary endothelial cells are fully resistant to TNF-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis. Here, we demonstrate that certain environmental conditions, such as exposure to the widespread allergen nickel, can dramatically increase the susceptibility of naturally resistant primary endothelial cells or keratinocytes to TRAIL-induced apoptosis. While nickel treatment increased surface expression of the apoptosis-inducing TRAIL receptors TRAIL-R1 and TRAIL-R2, it also up-regulated the apoptosis-deficient TRAIL-R4, suggesting that modulation of TRAIL receptor expression alone is unlikely to fully account for the dramatic sensitization effect of nickel. Further analysis of candidate mediators revealed that nickel strongly repressed c-FLIP at mRNA and protein levels. Accordingly, increased activation of Caspase-8 and Caspase-3 following nickel treatment was observed. Importantly, depletion of c-FLIP by RNA interference could largely recapitulate the effect of nickel and sensitize endothelial cells to TRAIL-dependent apoptosis in the absence of nickel pre-treatment. Conversely, ectopic expression of c-FLIP(L) largely protected nickel-treated cells from TRAIL-mediated apoptosis. Our data demonstrate that one key mechanism of sensitization of primary human endothelial cells or keratinocytes is transcriptional down-regulation of c-FLIP. We hypothesize that environmental factors, exemplified by the contact allergen nickel, strongly modulate death ligand sensitivity of endothelial cells and keratinocytes thus influencing vascular and epidermal function and integrity under physiological and pathophysiological conditions.
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