ArticleMolecular medicine reports2018
Extracellular matrix promotes proliferation, migration and adhesion of airway smooth muscle cells in a rat model of chronic obstructive pulmonary disease via upregulation of the PI3K/AKT signaling pathway.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
31 citing papers in PubMed, 51 citations in OpenAlex.
- Complement factor D regulates collagen type I expression and fibroblast migration to enhance human tendon repair and healing outcomes.Frontiers in immunology · 2023Trial
- Prognostic Predictors of Bronchial Thermoplasty for Symptom Control in Severe Asthma.Journal of asthma and allergy · 2026Article
- Qufeng Jiejing formula ameliorated the injury of airway smooth muscle cells induced by platelet-derived growth factor-BB through the transforming growth factor-β1/Smads signaling pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Cellular and Molecular Effects of the Bruck Syndrome-Associated Mutation in theInternational journal of molecular sciences · 2024Article
- Uncovering the action mechanism of Shenqi Tiaoshen formula in the treatment of chronic obstructive pulmonary disease through network pharmacology, molecular docking, and experimental verification.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- SHP-1 mediates cigarette smoke extract-induced epithelial-mesenchymal transformation and inflammation in 16HBE cells.Open medicine (Warsaw, Poland) · 2024Article
- Upregulated TIMP1 facilitates and coordinates myometrial contraction by decreasing collagens and cell adhesive capacity during human labor.Molecular human reproduction · 2023Article
- Exploring the Core Prescription and Underlying Mechanism of Traditional Chinese Medicine in Treating Allergic Rhinitis in Children: A Real- World Study Based on an Illustrious Senior Traditional Chinese Medicine Practitioner.Combinatorial chemistry & high throughput screening · 2023Article
- Targeting protein glycosylation to regulate inflammation in the respiratory tract: novel diagnostic and therapeutic candidates for chronic respiratory diseases.Frontiers in immunology · 2023Review
- Extracellular Vesicles' Role in the Pathophysiology and as Biomarkers in Cystic Fibrosis and COPD.International journal of molecular sciences · 2022Review
- Cellular Senescence in Aging Lungs and Diseases.Cells · 2022Review
- Transcriptomic analysis and validation reveal the pathogenesis and a novel biomarker of acute exacerbation of chronic obstructive pulmonary disease.Respiratory research · 2022Article
- Associative analysis of multi-omics data indicates that acetylation modification is widely involved in cigarette smoke-induced chronic obstructive pulmonary disease.Frontiers in medicine · 2022Article
- Transcription Factor p300 Regulated miR-451b Weakens the Cigarette Smoke Extract-Induced Cellular Stress by Targeting RhoA/ROCK2 Signaling.Oxidative medicine and cellular longevity · 2022Article
- Qufeng Xuanbi Formula Ameliorates Airway Remodeling in Asthmatic Mice by Suppressing Airway Smooth Muscle Cell Proliferation through MEK/ERK Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Emodin inhibits viability, proliferation and promotes apoptosis of hypoxic human pulmonary artery smooth muscle cells via targeting miR-244-5p/DEGS1 axis.BMC pulmonary medicine · 2021Article
- FGF gene expression in injured tendons as a prognostic biomarker of 1-year patient outcome after Achilles tendon repair.Journal of experimental orthopaedics · 2021Article
- Syndecan-1 Shedding by Matrix Metalloproteinase-9 Signaling Regulates Alveolar Epithelial Tight Junction in Lipopolysaccharide-Induced Early Acute Lung Injury.Journal of inflammation research · 2021Article
- NOX4-Derived ROS Promotes Collagen I Deposition in Bronchial Smooth Muscle Cells by Activating Noncanonical p38MAPK/Akt-Mediated TGF-Oxidative medicine and cellular longevity · 2021Article
- Emerging Role of Dermal White Adipose Tissue in Modulating Hair Follicle Development During Aging.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extracellular matrix (ECM) creates the tissue microenvironment and serves a role in airway wall remodeling in chronic obstructive pulmonary disease (COPD). However, the biological function of ECM in COPD remains to be elucidated. In the present study, 24 healthy Sprague Dawley rats were randomized to normal and COPD groups. COPD was established by intratracheal injection with lipopolysaccharide over 30 days. Subsequently, airway smooth muscle cells (ASMCs) were isolated from rats and served as a model to assess the effects of three ECM components, including collagen type I, laminin and collagen type III (COL‑3). Functional analysis in vitro, using cell counting kit‑8, flow cytometry, wound healing and cell adhesion assays indicated that the ECM components could promote cell proliferation, cell cycle progression, migration and adhesion ability, respectively. Furthermore, as demonstrated by ELISA, treatment with ECM components increased levels of C‑X‑C motif chemokine ligand 1 (CXCL1), CXCL8 and interleukin‑6 in ASMCs. Expression of transforming growth factor β1 (TGFβ1), fibroblast growth factor‑1 (FGF‑1) and tissue inhibitor of metalloproteinase 1 (TIMP1) was increased, and expression of matrix metalloproteinase‑9 (MMP‑9) was decreased following treatment with ECM components, as demonstrated by reverse transcription‑quantitative polymerase chain reaction and western blot analysis. Additionally, specific activation of phosphoinositide 3‑kinase (PI3K) signaling, using insulin‑like growth factor‑1 (IGF‑1), promoted cell proliferation and cell cycle progression, increased expression of TGFβ1, FGF‑1, PI3K, AKT, phospho‑AKT, serine/threonine‑protein kinase mTOR (mTOR), phospho‑mTOR and TIMP1, promoted cell migration capacity and reduced the expression level of MMP‑9 in cells from COPD rats. Consistently, PI3K inhibitor LY294002 exerted the opposite effect to IGF‑1. In conclusion, ECM proteins promoted proliferation, migration and adhesion of ASMCs form rat models of COPD through activation of the PI3K/AKT signaling pathway.
Indexed as
Identifiers
What OpenQuestion holds
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.