ArticlePloS one2011
Proteasome inhibition represses unfolded protein response and Nox4, sensitizing vascular cells to endoplasmic reticulum stress-induced death.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 42 citations in OpenAlex.
- Proteasome Inhibition Amplifies Endoplasmic Reticulum (ER) Stress Responses: Comparative Proteomics of Chinese Hamster Ovary Cell Lines.Biomolecules · 2026Article
- Endoplasmic reticulum stress in non-small cell lung cancer: a review of therapeutic agents, mechanistic insights, and implications for therapy.Frontiers in cell and developmental biology · 2025Review
- NADPH Oxidase 3: Beyond the Inner Ear.Antioxidants (Basel, Switzerland) · 2024Review
- Dynamic alteration in miRNA and mRNA expression profiles at different stages of chronic arsenic exposure-induced carcinogenesis in a human cell culture model of skin cancer.Archives of toxicology · 2021Article
- The Relationship of NADPH Oxidases and Heme Peroxidases: Fallin' in and Out.Frontiers in immunology · 2019Review
- C9ORF72 GGGGCC repeat-associated non-AUG translation is upregulated by stress through eIF2α phosphorylation.Nature communications · 2018Article
- Control of Amino Acid Homeostasis by a Ubiquitin Ligase-Coactivator Protein Complex.The Journal of biological chemistry · 2017Article
- Article
- The unfolded protein response and the phosphorylations of activating transcription factor 2 in the trans-activation of il23a promoter produced by β-glucans.The Journal of biological chemistry · 2014Article
- Nox NADPH oxidases and the endoplasmic reticulum.Antioxidants & redox signaling · 2014Review
- Cellular unfolded protein response against viruses used in gene therapy.Frontiers in microbiology · 2014Review
- Reactive oxygen species, vascular Noxs, and hypertension: focus on translational and clinical research.Antioxidants & redox signaling · 2014Review
- Article
- Endoplasmic reticulum stress-induced PCD and caspase-like activities involved.Frontiers in plant science · 2014Review
- Nitric oxide scavenging causes remodeling of the endoplasmic reticulum, Golgi apparatus and mitochondria in pulmonary arterial endothelial cells.Nitric oxide : biology and chemistry · 2013Article
- Role of nicotinamide adenine dinucleotide phosphate-reduced oxidase proteins in Pseudomonas aeruginosa-induced lung inflammation and permeability.American journal of respiratory cell and molecular biology · 2013Article
- Oxidative activation of Ca(2+)/calmodulin-activated kinase II mediates ER stress-induced cardiac dysfunction and apoptosis.American journal of physiology. Heart and circulatory physiology · 2013Article
- An involvement of oxidative stress in endoplasmic reticulum stress and its associated diseases.International journal of molecular sciences · 2012Review
- Molecular signatures of amyotrophic lateral sclerosis disease progression in hind and forelimb muscles of an SOD1(G93A) mouse model.Antioxidants & redox signaling · 2012Article
- Differential roles of NADPH oxidases in vascular physiology and pathophysiology.Frontiers in bioscience (Scholar edition) · 2012Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEndoplasmic reticulum (ER) stress has pathophysiological relevance in vascular diseases and merges with proteasome function. Proteasome inhibition induces cell stress and may have therapeutic implications. However, whether proteasome inhibition potentiates ER stress-induced apoptosis and the possible mechanisms involved in this process are unclear. METHODOLOGY/PRINCIPAL
findingsHere we show that proteasome inhibition with MG132, per se at non-lethal levels, sensitized vascular smooth muscle cells to caspase-3 activation and cell death during ER stress induced by tunicamycin (Tn). This effect was accompanied by suppression of both proadaptive (KDEL chaperones) and proapoptotic (CHOP/GADD153) unfolded protein response markers, although, intriguingly, the splicing of XBP1 was markedly enhanced and sustained. In parallel, proteasome inhibition completely prevented ER stress-induced increase in NADPH oxidase activity, as well as increases in Nox4 isoform and protein disulfide isomerase mRNA expression. Increased Akt phosphorylation due to proteasome inhibition partially offset the proapoptotic effect of Tn or MG132. Although proteasome inhibition enhanced oxidative stress, reactive oxygen species scavenging had no net effect on sensitization to Tn or MG132-induced cell death. CONCLUSION/RELEVANCE: These data indicate unfolded protein response-independent pathways whereby proteasome inhibition sensitizes vascular smooth muscle to ER stress-mediated cell death. This may be relevant to understand the therapeutic potential of such compounds in vascular disease associated with increased neointimal hyperplasia.
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