ArticleJournal of cellular physiology2021
Human antigen R promotes lung fibroblast differentiation to myofibroblasts and increases extracellular matrix production.
Article in Journal of cellular physiology, 2021. 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, 28 citations in OpenAlex.
- LncRNA RNF144A-AS1 increases P300-mediated H4K5 acetylation of PDE4 to promote keloid fibrosis.Biomedical engineering online · 2026Article
- Single-cell profiling reveals lineage-specific fibroblast stromal subtypes drive ECM remodeling and immune modulation in the hepatocellular carcinoma tumor microenvironment.Medical oncology (Northwood, London, England) · 2026Article
- DENetwork unveils non-differentially expressed genes with functional relevance across conditions through information flow perturbation.Nucleic acids research · 2025Article
- Research on tracheal stenosis based on molecular biomarkers.BMC pulmonary medicine · 2025Article
- In Vitro Anti-Aging Effects of Yeast/Rice Fermentation Filtrate Combined with Sialic Acid in Cosmetic Applications.Antioxidants (Basel, Switzerland) · 2025Article
- Novel Integration of Spatial and Single-Cell Omics Data Sets Enables Deeper Insights into IPF Pathogenesis.Proteomes · 2025Article
- Five New Indole Alkaloid Derivatives from Deep-Sea FungusMarine drugs · 2024Article
- Human Periodontal Ligament Stem Cells (hPDLSCs) Spontaneously Differentiate into Myofibroblasts to Repair Diabetic Wounds.Bioengineering (Basel, Switzerland) · 2024Article
- Fibroblast-Specific Depletion of Human Antigen R Alleviates Myocardial Fibrosis Induced by Cardiac Stress.JACC. Basic to translational science · 2024Article
- A2B Adenosine Receptor in Idiopathic Pulmonary Fibrosis: Pursuing Proper Pit Stop to Interfere with Disease Progression.International journal of molecular sciences · 2023Review
- Targeting HuR-Vav3 mRNA interaction prevents Pseudomonas aeruginosa adhesion to the cystic fibrosis airway epithelium.JCI insight · 2023Article
- Canadian Contributions in Fibroblast Biology.Cells · 2022Review
- Inhibition of RUNX1 blocks the differentiation of lung fibroblasts to myofibroblasts.Journal of cellular physiology · 2022Article
- Idiopathic pulmonary fibrosis: Current and future treatment.The clinical respiratory journal · 2022Review
- Characterizing cellular heterogeneity in fibrotic hypersensitivity pneumonitis by single-cell transcriptional analysis.Cell death discovery · 2022Article
- Drug delivery approaches for HuR-targeted therapy for lung cancer.Advanced drug delivery reviews · 2022Review
- Identification of Hub Genes in Idiopathic Pulmonary Fibrosis and NSCLC Progression:Evidence From Bioinformatics Analysis.Frontiers in genetics · 2022Article
- Blood biomarkers representing maternal-fetal interface tissues used to predict early-and late-onset preeclampsia but not COVID-19 infection.Computational and structural biotechnology journal · 2022Article
- HuR drives lung fibroblast differentiation but not metabolic reprogramming in response to TGF-β and hypoxia.Respiratory research · 2021Article
- Cell type-specific transforming growth factor-β (TGF-β) signaling in the regulation of salivary gland fibrosis and regeneration.Journal of oral biology and craniofacial researchArticle
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a disease of progressive scarring caused by excessive extracellular matrix (ECM) deposition and activation of α-SMA-expressing myofibroblasts. Human antigen R (HuR) is an RNA binding protein that promotes protein translation. Upon translocation from the nucleus to the cytoplasm, HuR functions to stabilize messenger RNA (mRNA) to increase protein levels. However, the role of HuR in promoting ECM production, myofibroblast differentiation, and lung fibrosis is unknown. Human lung fibroblasts (HLFs) treated with transforming growth factor β1 (TGF-β1) showed a significant increase in translocation of HuR from the nucleus to the cytoplasm. TGF-β-treated HLFs that were transfected with HuR small interfering RNA had a significant reduction in α-SMA protein as well as the ECM proteins COL1A1, COL3A, and FN1. HuR was also bound to mRNA for ACTA2, COL1A1, COL3A1, and FN. HuR knockdown affected the mRNA stability of ACTA2 but not that of the ECM genes COL1A1, COL3A1, or FN. In mouse models of pulmonary fibrosis, there was higher cytoplasmic HuR in lung structural cells compared to control mice. In human IPF lungs, there was also more cytoplasmic HuR. This study is the first to show that HuR in lung fibroblasts controls their differentiation to myofibroblasts and consequent ECM production. Further research on HuR could assist in establishing the basis for the development of new target therapy for fibrotic diseases, such as IPF.
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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 Socratic graph.