ArticleExperimental lung research2013
Thrombin induces epithelial-mesenchymal transition via PAR-1, PKC, and ERK1/2 pathways in A549 cells.
Article in Experimental lung research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Molecular Systems Architecture of Fibrotic Lung Microenvironment in Idiopathic Pulmonary Fibrosis.Cells · 2026Pooled it
- Disruption of perinatal myeloid niches impacts the aging clock of pancreatic β cells.iScience · 2024Article
- Role and targeting of the AGC kinase family in pulmonary fibrosis (Review).Experimental and therapeutic medicine · 2024Review
- Mechanism of Hirudin-Mediated Inhibition of Proliferation in Ovarian Cancer Cells.Molecular biotechnology · 2024Article
- Thrombin Induces COX-2 and PGEMediators of inflammation · 2022Article
- Effect of supercritical carbon dioxide fluid extract from Chrysanthemum indicum Linné on bleomycin-induced pulmonary fibrosis.BMC complementary medicine and therapies · 2021Article
- KLK8 promotes the proliferation and metastasis of colorectal cancer via the activation of EMT associated with PAR1.Cell death & disease · 2021Article
- Proteinase-activated receptor 1: A target for repurposing in the treatment of COVID-19?British journal of pharmacology · 2020Article
- MicroRNA Signature of Epithelial-Mesenchymal Transition in Group B Streptococcal Infection of the Placental Chorioamniotic Membranes.The Journal of infectious diseases · 2020Article
- Twist-mediated PAR1 induction is required for breast cancer progression and metastasis by inhibiting Hippo pathway.Cell death & disease · 2020Article
- Thrombin Upregulates PAI-1 and Mesothelial-Mesenchymal Transition Through PAR-1 and Contributes to Tuberculous Pleural Fibrosis.International journal of molecular sciences · 2019Article
- Protease-activated receptor-1 contributes to renal injury and interstitial fibrosis during chronic obstructive nephropathy.Journal of cellular and molecular medicine · 2019Article
- TRB3 regulates pulmonary interstitial fibrosis through the MAPK signaling pathway.International journal of clinical and experimental pathology · 2019Article
- A combined marker based on plasma D-dimer and serum albumin levels in patients with nasopharyngeal carcinoma is associated with poor survival outcomes in a retrospective cohort study.Journal of Cancer · 2019Article
- Antithrombotic Agents and Cancer.Cancers · 2018Review
- TGFβ upregulates PAR-1 expression and signalling responses in A549 lung adenocarcinoma cells.Oncotarget · 2016Article
- Stanniocalcin-1 inhibits thrombin-induced signaling and protects from bleomycin-induced lung injury.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thrombin activates protease-activated receptor (PAR)-1 and induces a myofibroblast phenotype in normal lung fibroblasts. The origins of myofibroblasts are resident fibroblasts, fibrocytes, and epithelial-mesenchymal transition (EMT). We investigated the effects of thrombin, an important mediator of interstitial lung fibrosis, on EMT in A549 human alveolar epithelial cells. We show that thrombin induced EMT and collagen I secretion through the activation of PAR-1, and PKC and ERK1/2 phosphorylation in A549 cells. These effects were largely prevented by a specific PAR-1 antagonist, short interfering RNA (siRNA) directed against PAR-1, or specific PKCα/β, δ, and ε inhibitors. These data indicated that interaction with thrombin and alveolar epithelial cells might directly contribute to the pathogenesis of pulmonary fibrosis through EMT. Targeting PAR-1 on the pulmonary epithelium or specific inhibitors to PKCα/β, δ, and ε might stop the fibrotic processes in human idiopathic pulmonary fibrosis by preventing thrombin-induced EMT.
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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.