ArticlePloS one2018
Crucial role of RAGE in inappropriate increase of smooth muscle cells from patients with pulmonary arterial hypertension.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- A review on clinical implications of S100 proteins in lung diseases.Frontiers in medicine · 2025Review
- Multimodal Screening for Pulmonary Arterial Hypertension in Systemic Scleroderma: Current Methods and Future Directions.Medicina (Kaunas, Lithuania) · 2024Review
- Advances in the study of S100A9 in cardiovascular diseases.Cell proliferation · 2024Review
- The soluble receptor for advanced glycation end products is potentially predictive of pulmonary arterial hypertension in systemic sclerosis.Frontiers in immunology · 2023Article
- Stem cell therapy for pulmonary arterial hypertension: An update.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2022Review
- IL-33/ST2 receptor-dependent signaling in the development of pulmonary hypertension in Sugen/hypoxia mice.Physiological reports · 2022Article
- Regulatory T Cell-Related Gene Indicators in Pulmonary Hypertension.Frontiers in pharmacology · 2022Article
- Soluble Receptor for Advanced Glycation End Products (sRAGE) Is a Sensitive Biomarker in Human Pulmonary Arterial Hypertension.International journal of molecular sciences · 2021Article
- Immunometabolic bases of type 2 diabetes in the severity of COVID-19.World journal of diabetes · 2021Review
- Intravenous Delivery of Lung-Targeted Nanofibers for Pulmonary Hypertension in Mice.Advanced healthcare materials · 2021Article
- Identifying early pulmonary arterial hypertension biomarkers in systemic sclerosis: machine learning on proteomics from the DETECT cohort.The European respiratory journal · 2021Article
- Identification of biomarkers and pathways for the SARS-CoV-2 infections that make complexities in pulmonary arterial hypertension patients.Briefings in bioinformatics · 2021Article
- Calprotectin in Lung Diseases.International journal of molecular sciences · 2021Review
- The heterodimer S100A8/A9 is a potent therapeutic target for idiopathic pulmonary fibrosis.Journal of molecular medicine (Berlin, Germany) · 2021Article
- Necrosis-Released HMGB1 (High Mobility Group Box 1) in the Progressive Pulmonary Arterial Hypertension Associated With Male Sex.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Vascular permeability disruption explored in the proteomes of mouse lungs and human microvascular cells following acute bromine exposure.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- SARS-CoV-2-mediated inflammatory response in lungs: should we look at RAGE?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Article
- World Trade Center-Cardiorespiratory and Vascular Dysfunction: Assessing the Phenotype and Metabolome of a Murine Particulate Matter Exposure Model.Scientific reports · 2020Article
- Current Treatment Strategies and Nanoparticle-Mediated Drug Delivery Systems for Pulmonary Arterial Hypertension.International journal of molecular sciences · 2019Review
- Cilostazol inhibits hyperglucose-induced vascular smooth muscle cell dysfunction by modulating the RAGE/ERK/NF-κB signaling pathways.Journal of biomedical science · 2019Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPulmonary vascular remodeling of pulmonary arterial hypertension (PAH) is characterized by an inappropriate increase of vascular cells. The receptor for advanced glycation end products (RAGE) is a type I single-pass transmembrane protein belonging to the immunoglobulin superfamily and is involved in a broad range of hyperproliferative diseases. RAGE is also implicated in the etiology of PAH and is overexpressed in pulmonary artery smooth muscle cells (PASMCs) in patients with PAH. We examined the role of RAGE in the inappropriate increase of PASMCs in patients with PAH. METHODS AND
resultsPASMCs were obtained from 12 patients with PAH including 9 patients with idiopathic PAH (IPAH) and 3 patients with heritable PAH (HPAH) (2 patients with BMPR2 mutation and one patient with SMAD9 mutation) who underwent lung transplantation. Western blot analysis and immunofluorescence staining revealed that RAGE and S100A8 and A9, ligands of RAGE, were overexpressed in IPAH and HPAH-PASMCs in the absence of any external growth stimulus. PDGF-BB (10 ng/mL) up-regulated the expression of RAGE in IPAH and HPAH-PASMCs. PAH-PASMCs are hyperplastic in the absence of any external growth stimulus as assessed by 3H-thymidine incorporation. This result indicates overgrowth characterized by continued growth under a condition of no growth stimulation in PAH-PASMCs. PDGF-BB stimulation caused a higher growth rate of PAH-PASMCs than that of non-PAH-PASMCs. AS-1, an inhibitor of TIR domain-mediated RAGE signaling, significantly inhibited overgrowth characterized by continued growth under a condition of no growth stimulation in IPAH and HPAH-PASMCs (P<0.0001). Furthermore, AS-1 significantly inhibited PDGF-stimulated proliferation of IPAH and HPAH-PASMCs (P<0.0001).
conclusionsRAGE plays a crucial role in the inappropriate increase of PAH-PASMCs. Inhibition of RAGE signaling may be a new therapeutic strategy for PAH.
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