ArticleJournal of immunology (Baltimore, Md. : 1950)2010
HLA-B35 upregulates endothelin-1 and downregulates endothelial nitric oxide synthase via endoplasmic reticulum stress response in endothelial cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 49 citations in OpenAlex.
- Endoplasmic Reticulum Stress: A Novel Target for the Prevention and Treatment of Hypertension and Its Related Diseases.Journal of cellular and molecular medicine · 2025Review
- HLA polymorphisms in South Tunisian systemic sclerosis patients: a case-control study.Clinical rheumatology · 2025Article
- HLA class I associations with the severity of COVID-19 disease in the United Arab Emirates.PloS one · 2023Article
- Kidney Involvement in Systemic Sclerosis.Journal of personalized medicine · 2022Review
- HLA repertoire of 115 UAE nationals infected with SARS-CoV-2.Human immunology · 2022Article
- Fibrillary Glomerulonephritis, DNAJB9, and the Unfolded Protein Response.Glomerular diseases · 2022Review
- Renal disorders in rheumatologic diseases: the spectrum is changing (Part 1: connective tissue diseases).Journal of nephrology · 2021Review
- Effects of Escitalopram on Endoplasmic Reticulum Stress and Oxidative Stress Induced by Tunicamycin.Frontiers in neuroscience · 2021Article
- HLA Expression Correlates to the Risk of Immune Checkpoint Inhibitor-Induced Pneumonitis.Cells · 2020Article
- AQP1 suppression by ATF4 triggers trabecular meshwork tissue remodelling in ET-1-induced POAG.Journal of cellular and molecular medicine · 2020Article
- A crucial role of endoplasmic reticulum stress in cellular responses during pulmonary arterial hypertension.American journal of translational research · 2020Review
- The Role of Protein Tyrosine Phosphatase (PTP)-1B in Cardiovascular Disease and Its Interplay with Insulin Resistance.Biomolecules · 2019Review
- Endoplasmic Reticulum Stress: A Critical Molecular Driver of Endothelial Dysfunction and Cardiovascular Disturbances Associated with Diabetes.International journal of molecular sciences · 2019Review
- Endoplasmic Reticulum Stress, a Driver or an Innocent Bystander in Endothelial Dysfunction Associated with Hypertension?Current hypertension reports · 2017Review
- Anti-Fibrotic Effect of Losartan, an Angiotensin II Receptor Blocker, Is Mediated through Inhibition of ER Stress via Up-Regulation of SIRT1, Followed by Induction of HO-1 and Thioredoxin.International journal of molecular sciences · 2017Article
- Role of endoplasmic reticulum stress signalling in diabetic endothelial dysfunction and atherosclerosis.Diabetes & vascular disease research · 2017Review
- Causes and consequences of endoplasmic reticulum stress in rheumatic disease.Nature reviews. Rheumatology · 2017Review
- The HLA-B*35 allele modulates ER stress, inflammation and proliferation in PBMCs from Limited Cutaneous Systemic Sclerosis patients.Arthritis research & therapy · 2015Article
- Pathogenesis of Systemic Sclerosis.Frontiers in immunology · 2015Review
- Mechanism of endoplasmic reticulum stress-induced vascular endothelial dysfunction.Biochimica et biophysica acta · 2014Article
Corrections and comments
- Retraction · 2021-05-27Duplication of/in Image · Falsification/Fabrication of Image · Investigation by Company/Institution · Original Data and/or Images not Provided and/or not Available ·
- Retracted
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
The presence of the HLA-B35 allele has emerged as an important risk factor for the development of isolated pulmonary hypertension in patients with scleroderma, however the mechanisms underlying this association have not been fully elucidated. The goal of our study was to determine the molecular mechanisms that mediate the biological effects of HLA-B35 in endothelial cells (ECs). Our data demonstrate that HLA-B35 expression at physiological levels via adenoviral vector resulted in significantly increased endothelin-1 (ET-1) and a significantly decreased endothelial NO synthase (eNOS), mRNA, and protein levels. Furthermore, HLA-B35 greatly upregulated expression of chaperones, including heat shock proteins (HSPs) HSP70 (HSPA1A and HSPA1B) and HSP40 (DNAJB1 and DNAJB9), suggesting that HLA-B35 induces the endoplasmic reticulum (ER) stress and unfolded protein response in ECs. Examination of selected mediators of the unfolded protein response, including H chain binding protein (BiP; GRP78), C/Ebp homologous protein (CHOP; GADD153), endoplasmic reticulum oxidase, and protein disulfide isomerase has revealed a consistent increase of BiP expression levels. Accordingly, thapsigargin, a known ER stress inducer, stimulated ET-1 mRNA and protein levels in ECs. This study suggests that HLA-B35 could contribute to EC dysfunction via ER stress-mediated induction of ET-1 in patients with pulmonary hypertension.
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Registered trials
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.