FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1992558298> ?p ?o ?g. }

• W1992558298 endingPage "318" @default.
• W1992558298 startingPage "307" @default.
• W1992558298 abstract "Cadmium (Cd) is a toxic metal with multiple effects on cell signaling and cell death. We studied the effects of Cd2+ on quiescent mouse mesangial cells in serum-free conditions. Cadmium induces cell death over 6 h through annexin V+ states without or with causing uptake of propidium iodide, termed apoptotic and apoptosis-like death, respectively. Little or no necrosis is observed, and cell death is caspase-independent and associated with nuclear translocation of the apoptosis-inducing factor, AIF. We previously showed that Cd2+ increased phosphorylation of Erk and CaMK-II, and CaMK-II activation increased cell death in an Erk-independent manner. Here we demonstrate that Cd2+ increases Jnk and p38 kinase phosphorylation, and inhibition of p38—but not of Jnk—increases cell viability by suppressing apoptosis in preference to apoptosis-like death. Neither p38 kinase nor CaMK-II inhibition protects against a decrease in mitochondrial membrane potential, ψ, indicating that kinase-mediated death is either independent of, or involves events downstream of a mitochondrial pathway. However, both the antioxidant N-acetyl cysteine (NAC) and the mitochondrial membrane-stabilizing agent cyclosporine A (CsA) partially preserve ψ, suppress activation of p38 kinase, and partially protect the cells from Cd2+-induced death. Whereas the effect of CsA is on apoptosis, NAC acts on apoptosis-like death. Inhibition of glutathione synthesis exacerbates a Cd2+-dependent increase in cellular peroxides and favors apoptosis-like death over apoptosis. The caspase-independence of these modes of cell death is not due to an absence of this machinery in the mesangial cells: when they are exposed to Cd2+ for longer periods in the presence of serum, procaspase-3 and PARP are cleaved and caspase inhibition is protective. We conclude that Cd2+ can kill mesangial cells by multiple pathways, including caspase-dependent and -independent apoptotic and apoptosis-like death. Necrosis is not prominent. Activation of p38 kinase and of CaMK-II by Cd2+ are associated with caspase-independent apoptosis that is not dependent on mitochondrial destabilization. J. Cell. Physiol. 217: 307–318, 2008. © 2008 Wiley-Liss, Inc." @default.
• W1992558298 created "2016-06-24" @default.
• W1992558298 creator A5041935017 @default.
• W1992558298 creator A5060002817 @default.
• W1992558298 date "2008-11-01" @default.
• W1992558298 modified "2023-10-03" @default.
• W1992558298 title "Initiation of caspase-independent death in mouse mesangial cells by Cd²⁺: Involvement of p38 kinase and CaMK-II" @default.
• W1992558298 cites W1565531261 @default.
• W1992558298 cites W18766598 @default.
• W1992558298 cites W1904882776 @default.
• W1992558298 cites W1965341477 @default.
• W1992558298 cites W1968601094 @default.
• W1992558298 cites W1971253447 @default.
• W1992558298 cites W1977446960 @default.
• W1992558298 cites W1979132200 @default.
• W1992558298 cites W1979427782 @default.
• W1992558298 cites W198362610 @default.
• W1992558298 cites W2004051386 @default.
• W1992558298 cites W2016537201 @default.
• W1992558298 cites W2017836748 @default.
• W1992558298 cites W2018509996 @default.
• W1992558298 cites W2019506696 @default.
• W1992558298 cites W2020913460 @default.
• W1992558298 cites W2025194227 @default.
• W1992558298 cites W2028637690 @default.
• W1992558298 cites W2029764326 @default.
• W1992558298 cites W2031890209 @default.
• W1992558298 cites W2034915619 @default.
• W1992558298 cites W2035554117 @default.
• W1992558298 cites W2035736023 @default.
• W1992558298 cites W2035981095 @default.
• W1992558298 cites W2037067089 @default.
• W1992558298 cites W2044781471 @default.
• W1992558298 cites W2045943113 @default.
• W1992558298 cites W2057655548 @default.
• W1992558298 cites W2060159866 @default.
• W1992558298 cites W2060344069 @default.
• W1992558298 cites W2067084274 @default.
• W1992558298 cites W2068890239 @default.
• W1992558298 cites W2073414552 @default.
• W1992558298 cites W2073469304 @default.
• W1992558298 cites W2074577245 @default.
• W1992558298 cites W2078515286 @default.
• W1992558298 cites W2092118074 @default.
• W1992558298 cites W2112173647 @default.
• W1992558298 cites W2123765743 @default.
• W1992558298 cites W2131498907 @default.
• W1992558298 cites W2135203759 @default.
• W1992558298 cites W2139366028 @default.
• W1992558298 cites W2141181325 @default.
• W1992558298 cites W2166649538 @default.
• W1992558298 cites W2171501507 @default.
• W1992558298 cites W4230920228 @default.
• W1992558298 doi "https://doi.org/10.1002/jcp.21499" @default.
• W1992558298 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18506790" @default.
• W1992558298 hasPublicationYear "2008" @default.
• W1992558298 type Work @default.
• W1992558298 sameAs 1992558298 @default.
• W1992558298 citedByCount "50" @default.
• W1992558298 countsByYear W19925582982012 @default.
• W1992558298 countsByYear W19925582982013 @default.
• W1992558298 countsByYear W19925582982014 @default.
• W1992558298 countsByYear W19925582982015 @default.
• W1992558298 countsByYear W19925582982016 @default.
• W1992558298 countsByYear W19925582982017 @default.
• W1992558298 countsByYear W19925582982018 @default.
• W1992558298 countsByYear W19925582982019 @default.
• W1992558298 countsByYear W19925582982020 @default.
• W1992558298 countsByYear W19925582982022 @default.
• W1992558298 countsByYear W19925582982023 @default.
• W1992558298 crossrefType "journal-article" @default.
• W1992558298 hasAuthorship W1992558298A5041935017 @default.
• W1992558298 hasAuthorship W1992558298A5060002817 @default.
• W1992558298 hasConcept C153911025 @default.
• W1992558298 hasConcept C184235292 @default.
• W1992558298 hasConcept C185592680 @default.
• W1992558298 hasConcept C190283241 @default.
• W1992558298 hasConcept C2775934118 @default.
• W1992558298 hasConcept C31573885 @default.
• W1992558298 hasConcept C51551487 @default.
• W1992558298 hasConcept C55493867 @default.
• W1992558298 hasConcept C57074206 @default.
• W1992558298 hasConcept C86803240 @default.
• W1992558298 hasConcept C88634738 @default.
• W1992558298 hasConcept C95444343 @default.
• W1992558298 hasConcept C98424977 @default.
• W1992558298 hasConceptScore W1992558298C153911025 @default.
• W1992558298 hasConceptScore W1992558298C184235292 @default.
• W1992558298 hasConceptScore W1992558298C185592680 @default.
• W1992558298 hasConceptScore W1992558298C190283241 @default.
• W1992558298 hasConceptScore W1992558298C2775934118 @default.
• W1992558298 hasConceptScore W1992558298C31573885 @default.
• W1992558298 hasConceptScore W1992558298C51551487 @default.
• W1992558298 hasConceptScore W1992558298C55493867 @default.
• W1992558298 hasConceptScore W1992558298C57074206 @default.
• W1992558298 hasConceptScore W1992558298C86803240 @default.
• W1992558298 hasConceptScore W1992558298C88634738 @default.
• W1992558298 hasConceptScore W1992558298C95444343 @default.

• next