ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013
Endothelin-1 receptor antagonists regulate cell surface-associated protein disulfide isomerase in sickle cell disease.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. 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, 32 citations in OpenAlex.
- Isoquercetin for thromboinflammation in sickle cell disease: a randomized double-blind placebo-controlled trial.Blood advances · 2024Trial
- Blockade of the mineralocorticoid receptor improves markers of human endothelial cell dysfunction and hematological indices in a mouse model of sickle cell disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Trial
- Targeting protein disulfide isomerase with the flavonoid isoquercetin to improve hypercoagulability in advanced cancer.JCI insight · 2019Trial
- Article
- Proteome alterations in erythrocytes with PIEZO1 gain-of-function mutations.Blood advances · 2023Article
- Blockade of endothelin-1 receptor B regulates molecules of the major histocompatibility complex in sickle cell disease.Frontiers in immunology · 2023Article
- Magnesium homeostasis in deoxygenated sickle erythrocytes is modulated by endothelin-1 via NaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Inhibitory effects of Syzygium jambos extract on biomarkers of endothelial cell activation.BMC complementary medicine and therapies · 2022Article
- Native structure of the RhopH complex, a key determinant of malaria parasite nutrient acquisition.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Protein disulfide isomerase plasma levels in healthy humans reveal proteomic signatures involved in contrasting endothelial phenotypes.Redox biology · 2019Article
- Therapeutic strategies for sickle cell disease: towards a multi-agent approach.Nature reviews. Drug discovery · 2019Review
- Article
- Efficient replication of a paramyxovirus independent of full zippering of the fusion protein six-helix bundle domain.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Aldosterone's rapid, nongenomic effects are mediated by striatin: a modulator of aldosterone's effect on estrogen action.Endocrinology · 2014Article
- Methods of measuring protein disulfide isomerase activity: a critical overview.Frontiers in chemistry · 2014Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Increased endothelin-1 (ET-1) levels, disordered thiol protein status, and erythrocyte hydration status play important roles in sickle cell disease (SCD) through unresolved mechanisms. Protein disulfide isomerase (PDI) is an oxidoreductase that mediates thiol/disulfide interchange reactions. We provide evidence that PDI is present in human and mouse erythrocyte membranes and that selective blockade with monoclonal antibodies against PDI leads to reduced Gardos channel activity (1.6±0.03 to 0.56±0.02 mmol·10(13) cell(-1)·min(-1), P<0.001) and density of sickle erythrocytes (D50: 1.115±0.001 to 1.104±0.001 g/ml, P=0.012) with an IC50 of 4 ng/ml. We observed that erythrocyte associated-PDI activity was increased in the presence of ET-1 (3.1±0.2 to 5.6±0.4%, P<0.0001) through a mechanism that includes casein kinase II. Consistent with these results, in vivo treatment of BERK sickle transgenic mice with ET-1 receptor antagonists lowered circulating and erythrocyte associated-PDI activity (7.1±0.3 to 5.2±0.2%, P<0.0001) while improving hematological parameters and Gardos channel activity. Thus, our results suggest that PDI is a novel target in SCD that regulates erythrocyte volume and oxidative stress and may contribute to cellular adhesion and endothelial activation leading to vasoocclusion as observed in SCD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.