Regular ArticleCalpain Contributes to Silica-Induced IκB-α Degradation and Nuclear Factor-κB Activation
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A Novel Mechanism for NF-kB-activation via IkB-aggregation: Implications for Hepatic Mallory-Denk-Body Induced Inflammation
2020, Molecular and Cellular ProteomicsCitation Excerpt :Thus, we excluded two such established mechanisms: (i) Translational suppression of IκBα upon activation of the heme-regulated inhibitor (HRI) eIF2α kinase through NMPP-elicited heme-deficiency, by documenting that HRI-genetic ablation failed to affect such NMPP-elicited IκBα-loss in mouse hepatocytes [(56); Figs. 1D and supplemental Fig. S2A]; and (ii) enhanced IκBα autophagy by documenting that such an IκBα-loss in MEF cells was unaffected by ATG5-knockout (KO) [(57); supplemental Fig. S2B]. Additionally, we also excluded two plausible mechanisms: (iii) Enhanced calpain-mediated proteolysis of IκBα by documenting that such a loss was unaffected in MEF cells upon genetic calpain-KO [(58); supplemental Fig.S2C]; and (iv) PPIX-photoactivation and consequent ROS-mediated oxidative stress (28) in NMPP-elicited IκBα-loss through the use of specific ROS scavengers, antioxidants and/or inhibitors (Supplemental Results; supplemental Fig. S3). Because NMPP-elicited ferrochelatase inhibition results in PPIX-accumulation, we examined whether this accumulation (and not heme deficiency per se) was mainly responsible for the observed IκBα-loss and NF-κB activation.
Calpeptin attenuates cigarette smoke-induced pulmonary inflammation via suppressing calpain/IκBα signaling in mice and BEAS-2B cells
2018, Pathology Research and PracticeCitation Excerpt :Individual differences in inflammatory response and differences in repair capacity of CS-induced destruction by reactive oxygen species were likely genetically inherent [31]. Calpains play an vital role in IκBα degradation to activate NF-кB in a T-cell activation model and non–T-cell models [32]. Calpains degraded silica-induced IκBα, then activated NF-кB but did not lead to lipopolysaccharide-induced IκBα degradation and NF-kB activation [32].
Bioactive sesquiterpenoids from the flowers of Inula japonica
2016, PhytochemistryCalpain-2 contributes to neuropathic pain following motor nerve injury via up-regulating interleukin-6 in DRG neurons
2015, Brain, Behavior, and ImmunityCitation Excerpt :In our in vivo study, we observed a dose-independent transient allodynia induced by rr-CALP2 (Fig. 6G–I), suggesting that calpain-2 might be a mediator but was not the only one to trigger pain. Calpain-2-mediated cascade responses, such as the activation of nuclear factor-kappa B (NF-κB) (Chen et al., 1997; Fenouille et al., 2012; Lee et al., 2005; Schaecher et al., 2004; Shumway et al., 1999) and the subsequent secretion of pro-inflammatory cytokines (Iguchi-Hashimoto et al., 2011; Uceyler et al., 2007) might play more important roles in the development of chronic pain (He et al., 2010; Wei et al., 2013a; Xu et al., 2006; Zang et al., 2010). Earlier studies have confirmed that the activity of calpain is able to be regulated by its association with its intrinsic inhibitor calpastatin (Guroff, 1964; Murachi et al., 1989).
Long-term incubation with proteasome inhibitors (PIs) induces IκBα degradation via the lysosomal pathway in an IκB kinase (IKK)-dependent and IKK-independent manner
2013, Journal of Biological ChemistryCitation Excerpt :There are several circumstances in which participation of other protein degradation systems have been described. The calcium-activated calpain system (25–26), caspases (27), lysosomes (28), and unknown proteinases have been suggested to be responsible for IκB degradation. In this study, lysosomal inhibitor (chloroquine or NH4Cl) and cathepsin inhibitors (Z-FF-FMK or Z-FA-FMK) suppressed PI-induced IκBα degradation, but did not affect TNF-α-mediated IκBα degradation in NCI-H157 cells and lipopolysaccharide (LPS) or CpG-oligodeooxynucleotide (CpG-ODN)-induced IκBα degradation in macrophage cell line (data not shown).
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