ArticleThe Biochemical journal1998
Thrombin stimulates fibroblast procollagen production via proteolytic activation of protease-activated receptor 1.
Article in The Biochemical journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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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
58 citing papers in PubMed, 156 citations in OpenAlex.
- The Advances in Novel Delivery Strategies for Hirudin Against Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2026Review
- The Intricate Relationship Between Pulmonary Fibrosis and Thrombotic Pathology: A Narrative Review.Cells · 2024Review
- Microvascular Thrombosis and Liver Fibrosis Progression: Mechanisms and Clinical Applications.Cells · 2023Review
- Immune Mechanisms of Pulmonary Fibrosis with Bleomycin.International journal of molecular sciences · 2023Review
- The Therapeutic Potential of Anticoagulation in Organ Fibrosis.Frontiers in medicine · 2022Review
- E-Selectin-Overexpressing Mesenchymal Stem Cell Therapy Confers Improved Reperfusion, Repair, and Regeneration in a Murine Critical Limb Ischemia Model.Frontiers in cardiovascular medicine · 2021Article
- Review
- GFOGER Peptide Modifies the Protein Content of Extracellular Vesicles and Inhibits Vascular Calcification.Frontiers in cell and developmental biology · 2020Article
- Hirudin ameliorates immunoglobulin A nephropathy by inhibition of fibrosis and inflammatory response.Renal failure · 2019Article
- Role of the coagulation system in the pathogenesis of sickle cell disease.Blood advances · 2019Article
- Safety and Tolerability of Thrombin Inhibition in Scleroderma-Associated Interstitial Lung Disease.ACR open rheumatology · 2019Article
- Elimination of the fibrinogen integrin αBlood advances · 2019Article
- Hematopoietic protease nexin-1 protects against lung injury by preventing thrombin signaling in mice.Blood advances · 2018Article
- Review
- The fibrotic tumor stroma.The Journal of clinical investigation · 2018Review
- Uncoupling of the profibrotic and hemostatic effects of thrombin in lung fibrosis.JCI insight · 2017Article
- High endogenous activated protein C levels attenuates bleomycin-induced pulmonary fibrosis.Journal of cellular and molecular medicine · 2016Article
- Fibroblast Activation Protein (FAP) Accelerates Collagen Degradation and Clearance from Lungs in Mice.The Journal of biological chemistry · 2016Article
- A priming dose of protons alters the early cardiac cellular and molecular response to (56)Fe irradiation.Life sciences in space research · 2016Article
- Phylogenomic and biogeographic reconstruction of the Trichinella complex.Nature communications · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Thrombin is a multifunctional serine protease that has a crucial role in blood coagulation. It is also a potent mesenchymal cell mitogen and chemoattractant and might therefore have an important role in the recruitment and local proliferation of mesenchymal cells at sites of tissue injury. We hypothesized that thrombin might also affect the deposition of connective tissue proteins at these sites by directly stimulating fibroblast procollagen production. To address this hypothesis, the effect of thrombin on procollagen production and gene expression by human foetal lung fibroblasts was assessed over 48 h. Thrombin stimulated procollagen production at concentrations of 1 nM and above, with maximal increases of between 60% and 117% at 10 nM thrombin. These effects of thrombin were, at least in part, due to increased steady-state levels of alpha1(I) procollagen mRNA. They could furthermore be reproduced with thrombin receptor-activating peptides for the protease-activated receptor 1 (PAR-1) and were completely abolished when thrombin was rendered proteolytically inactive with the specific inhibitors d-Phe-Pro-ArgCH2Cl and hirudin, indicating that thrombin is mediating these effects via the proteolytic activation of PAR-1. These results suggest that thrombin might influence the deposition of connective tissue proteins during normal wound healing and the development of tissue fibrosis by stimulating fibroblast procollagen production.
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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.