ArticleAmerican journal of respiratory cell and molecular biology2010
MicroRNA expression in human airway smooth muscle cells: role of miR-25 in regulation of airway smooth muscle phenotype.
Article in American journal of respiratory cell and molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
What it found
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The trial behind it
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Who cites it
78 citing papers in PubMed, 143 citations in OpenAlex.
- MicroRNAs-Are They Possible Markers of Allergic Diseases and Efficient Immunotherapy?International journal of molecular sciences · 2026Review
- Characterization and biological health implications of microRNAs from human milk and infant formulas.NPJ science of food · 2025Review
- ANXA13 expression patterns in hepatocellular carcinoma and impact on tumor behavior.World journal of gastrointestinal surgery · 2025Article
- Phenotypic Switching of VSMCs in the Development of CVDs: Focus on miRs.International journal of molecular sciences · 2025Review
- MACC1 ablation suppresses the dedifferentiation process of non-CSCs in lung cancer through stabilizing KLF4.Cell death discovery · 2024Article
- High-Throughput Quantification of miRNA-3'-Untranslated-Region Regulatory Effects.bioRxiv : the preprint server for biology · 2024Article
- Noncoding RNAs in asthmatic airway smooth muscle cells.European respiratory review : an official journal of the European Respiratory Society · 2023Review
- Review
- Human bone marrow-mesenchymal stem cell-derived exosomal microRNA-188 reduces bronchial smooth muscle cell proliferation in asthma through suppressing the JARID2/Wnt/β-catenin axis.Cell cycle (Georgetown, Tex.) · 2022Article
- Down-regulation of miR-140-3p is a cause of the interlukin-13-induced up-regulation of RhoA protein in bronchial smooth muscle cells.Small GTPases · 2022Article
- Six Shades of Vascular Smooth Muscle Cells Illuminated by KLF4 (Krüppel-Like Factor 4).Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- Interleukin-1β in Multifactorial Hypertension: Inflammation, Vascular Smooth Muscle Cell and Extracellular Matrix Remodeling, and Non-Coding RNA Regulation.International journal of molecular sciences · 2021Review
- Review
- Airway Epithelial Cells Drive Airway Smooth Muscle Cell Phenotype Switching to the Proliferative and Pro-inflammatory Phenotype.Frontiers in physiology · 2021Article
- MiR-502 Suppresses TNF-BioMed research international · 2021Article
- Downregulation of miR-140-3p Contributes to Upregulation of CD38 Protein in Bronchial Smooth Muscle Cells.International journal of molecular sciences · 2020Article
- Xeno-miRNA in Maternal-Infant Immune Crosstalk: An Aid to Disease Alleviation.Frontiers in immunology · 2020Review
- MicroRNAs: Potential Biomarkers and Targets of Therapy in Allergic Diseases?Archivum immunologiae et therapiae experimentalis · 2019Review
- Endoplasmic Reticulum Stress and Mitochondrial Function in Airway Smooth Muscle.Frontiers in cell and developmental biology · 2019Review
- Upregulation of LncRNA Malat1 Induced Proliferation and Migration of Airway Smooth Muscle CellsFrontiers in physiology · 2019Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Defining mechanisms by which differentiated, contractile smooth muscle cells become proliferative and secretory in response to mechanical and environmental stress is crucial for determining the contribution of airway smooth muscle (ASM) to inflammatory responses that result in airway disease. Regulation by microRNAs (miRNAs) has emerged as an important post-transcriptional mechanism regulating gene expression that may modulate ASM phenotype, but little is known about the expression and functions of miRNA in smooth muscle. In the present study we used microarrays to determine whether miRNAs in human ASM cells are altered by a proinflammatory stimulus. In ASM cells exposed to IL-1beta, TNF-alpha, and IFN-gamma, we found 11 miRNAs to be significantly down-regulated. We verified decreased expression of miR-25, miR-140*, mir-188, and miR-320 by quantitative PCR. Analysis of miR-25 expression indicates that it has a broad role in regulating ASM phenotype by modulating expression of inflammatory mediators such as RANTES, eotaxin, and TNF-alpha; genes involved in extracellular matrix turnover; and contractile proteins, most notably myosin heavy chain. miRNA binding algorithms predict that miR-25 targets Krüppel-like factor 4 (KLF4), a potent inhibitor of smooth muscle-specific gene expression and mediator of inflammation. Our study demonstrates that inhibition of miR-25 in cytokine-stimulated ASM cells up-regulates KLF4 expression via a post-transcriptional mechanism. This provides novel evidence that miR-25 targets KLF4 in ASM cells and proposes that miR-25 may be an important mediator of ASM phenotype.
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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.