Dual function of peroxiredoxin I in lipopolysaccharide-induced osteoblast apoptosis via reactive oxygen species and the apoptosis signal-regulating kinase 1 signaling pathway

Feng, Hao; Li, Ziyu; Du, Juan; Sun, Jing; Feng, Wei; Li, Dongfang; Liu, Shanshan; Wang, Wei; Liu, Hongrui; Amizuka, Norio; Li, Minqi

doi:10.1038/s41420-018-0050-9

Cited by 13 publications

(6 citation statements)

References 39 publications

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“…Taking into account the above, and the fact that long-term application of CBD reduces the severity of the antioxidant response, this may indicate a pro-apoptotic effect of this CBD application. Additionally, the increase in the levels of peroxiredoxin −1, −4, −5, and −6 adducts with 4-HNE in cells treated with CBD and UVB observed in this study may indicate dysfunction of these enzymes [ 46 ], which, according to the literature [ 47 ], may intensify pro-apoptotic signaling.…”

Section: Discussionmentioning

confidence: 74%

Protective Effects of Cannabidiol on the Membrane Proteome of UVB-Irradiated Keratinocytes

Atalay

Gęgotek

2021

Antioxidants

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Ultraviolet (UV) radiation contained in sunlight disturbs the redox state of skin cells, leading to changes in the structures and functions of macromolecules including components of biological membranes. Cannabidiol (CBD), which accumulates in biomembranes, may be a promising protective antioxidant compound. Accordingly, the aim of this study was to compare the effects of short-term (24 h) and long-term (48 h) CBD application on the proteomic profile of biological membranes in UVB-irradiated keratinocytes. The data obtained show that UVB radiation quantitatively and qualitatively modified cell membrane proteins, with a particular research focus on adducts of proteins with the lipid peroxidation products malondialdehyde (MDA) or 4-hydroxynonenal (4-HNE). CBD application reduced the UVB-enhanced level of these protein adducts. This was particularly notable amongst proteins related to cell proliferation and apoptosis. Moreover, CBD dramatically increased the UVB-induced expression of proteins involved in the regulation of protein translation and cell proliferation (S3a/L13a/L7a ribosomal proteins), the inflammatory response (S100/S100-A6 proteins), and maintenance of redox balance (peroxiredoxin-1, carbonyl reductase 1, and aldo-keto reductase family 1 members). In contrast, CBD effects on the level of 4-HNE-protein adducts involved in the antioxidant response and proteasomal degradation process indicate that CBD may protect keratinocytes in connection with protein catabolism processes or pro-apoptotic action.

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Section: Discussionmentioning

confidence: 74%

Protective Effects of Cannabidiol on the Membrane Proteome of UVB-Irradiated Keratinocytes

Atalay

Gęgotek

2021

Antioxidants

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“…SOD1, which catalyzes superoxide dismutation, was associated with H 2 O 2 production and also contributed to M2 alternative activation that was regulated by redox-dependent STAT6 translocation [ 53 ]. PRDX1 and PRDX5 exert protective effects on cellular toxicity against increased cellular H 2 O 2 levels induced by oxidative and inflammatory stresses [ 54 ]. Following oxidation of PRDX , they form disulfide linkages, while they return to their active form after reduction by TXN [ 55 ].…”

Section: Discussionmentioning

confidence: 99%

Proteomic profiling reveals engineered chitosan nanoparticles mediated cellular crosstalk and immunomodulation for therapeutic application in apical periodontitis

Hussein

Kishen

2022

Bioactive Materials

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Macrophages (MQ) are major constituents of chronically inflamed periapical tissues in apical periodontitis. This study aimed to investigate the immunomodulatory effect of engineered bioactive chitosan-based nanoparticles (CSnp) antibiofilm medication on MQ cocultured with periodontal ligament fibroblasts (PdLF). Cells viability, spreading, PdLF migration, and intracellular CSnp uptake were characterized. Tandem Mass Tag-based proteomics was applied to analyze MQ global protein expression profiles after interaction with Enterococcus faecalis biofilm, CSnp-treated biofilm, and CSnp. Secreted inflammatory mediators were analyzed. Following bioinformatics analyses, candidate proteins were validated via targeted proteomics. CSnp maintained cells viability, increased MQ spreading, and PdLF migration ( p < 0.05). Transmission electron micrographs demonstrated CSnp internalization via macropinocytosis, clathrin-mediated endocytosis, and phagocytosis. Proteomic analysis revealed that CSnp-treated biofilm upregulated proteins (>1.5-folds, p < 0.05) showed functional enrichment in the pathway of metal sequestration by antimicrobial proteins, while downregulated proteins showed enrichment in ferroptosis. CSnp upregulated proteins exhibiting antioxidant and immunoregulatory properties. Upregulation of SERPINB1 by CSnp (>1.5-folds, p < 0.05) was validated. CSnp-treated biofilm reduced pro-inflammatory IL-1β and nitric oxide but enhanced anti-inflammatory IL-10 and TGF-β1 ( p < 0.05). Internalized engineered bioactive CSnp reprogrammed MQ proteomic and cytokine profiles to modulate biofilm-mediated inflammation, and prompted PdLF migration, emphasizing its potential to regulate healing process in the treatment of apical periodontitis.

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“…There are several pathways which can trigger rat cardiomyocyte apoptosis and activation of caspase 3. The first is procaspase-9 activates Apaf-1/dATP/cytochrome c apoptotic bodies (Feng et al, 2018). The second is the NO/iNOS pathway (Chakravortty et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

The Role of HSP70 in the Protective Effects of NVP-AUY922 on Multiple Organ Dysfunction Syndrome in Endotoxemic Rats

et al. 2021

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Sepsis is defined as a life-threatening organ dysfunction syndrome with high morbidity and mortality caused by bacterial infection. The major characteristics of sepsis are systemic inflammatory responses accompanied with elevated oxidative stress, leading to multiple organ dysfunction syndrome (MODS), and disseminated intravascular coagulation (DIC). As a molecular chaperon to repair unfolded proteins, heat shock protein 70 (HSP70) maintains cellular homeostasis and shows protective effects on inflammatory damage. HSP 90 inhibitors were reported to exert anti-inflammatory effects via activation of the heat shock factor-1 (HSF-1), leading to induction of HSP70. We evaluated the beneficial effect of HSP 90 inhibitor NVP-AUY 922 (NVP) on multiple organ dysfunction syndrome induced by lipopolysaccharide (LPS) and further explored the underlying mechanism. NVP (5 mg/kg, i.p.) was administered 20 h prior to LPS initiation (LPS 30 mg/kg, i.v. infusion for 4 h) in male Wistar rats. Results demonstrated that pretreatment with NVP significantly increased survival rate and prevented hypotension at 6 h after LPS injection. Plasma levels of ALT, CRE and LDH as well as IL-1β and TNF-α were significantly reduced by NVP at 6 h after LPS challenge. The induction of inducible NO synthase in the liver, lung and heart and NF-κB p-p65 and caspase 3 protein expression in the heart were also attenuated by NVP. In addition, NVP markedly induced HSP70 and HO-1 proteins in the liver, lung and heart after LPS injection. These results indicated that NVP possessed the anti-inflammatory and antioxidant effects on LPS-induced acute inflammation, which might be associated with HSP70 and HO-1, leading to prevent MODS in sepsis. NVP might be considered as a novel therapeutic strategy in the prevention of sepsis-induced MODS.

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Dual function of peroxiredoxin I in lipopolysaccharide-induced osteoblast apoptosis via reactive oxygen species and the apoptosis signal-regulating kinase 1 signaling pathway

Cited by 13 publications

References 39 publications

Protective Effects of Cannabidiol on the Membrane Proteome of UVB-Irradiated Keratinocytes

Protective Effects of Cannabidiol on the Membrane Proteome of UVB-Irradiated Keratinocytes

Proteomic profiling reveals engineered chitosan nanoparticles mediated cellular crosstalk and immunomodulation for therapeutic application in apical periodontitis

The Role of HSP70 in the Protective Effects of NVP-AUY922 on Multiple Organ Dysfunction Syndrome in Endotoxemic Rats

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