ArticleMolecular medicine (Cambridge, Mass.)2014
Protease activated receptor-1 deficiency diminishes bleomycin-induced skin fibrosis.
Article in Molecular medicine (Cambridge, Mass.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Targeting thrombin with hirudin alleviates paraquat-induced pulmonary fibrosis via the PAR-1-mediated TGF-β1 pathway.Histology and histopathology · 2026Article
- Activated Protein C Protects against Murine Contact Dermatitis by Suppressing Protease-Activated Receptor 2.International journal of molecular sciences · 2022Article
- Advances in Understanding the Initial Steps of Pruritoceptive Itch: How the Itch Hits the Switch.International journal of molecular sciences · 2020Review
- Hirudin Ameliorates Renal Interstitial Fibrosis via Regulating TGF-Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Cell type-specific mechanisms coupling protease-activated receptor-1 to infectious colitis pathogenesis.Journal of thrombosis and haemostasis : JTH · 2020Article
- Protease-activated receptor-1 contributes to renal injury and interstitial fibrosis during chronic obstructive nephropathy.Journal of cellular and molecular medicine · 2019Article
- Signaling Crosstalk of TGF-β/ALK5 and PAR2/PAR1: A Complex Regulatory Network Controlling Fibrosis and Cancer.International journal of molecular sciences · 2018Review
- Vorapaxar treatment reduces mesangial expansion in streptozotocin-induced diabetic nephropathy in mice.Oncotarget · 2018Article
- High endogenous activated protein C levels attenuates bleomycin-induced pulmonary fibrosis.Journal of cellular and molecular medicine · 2016Article
- Protease-activated receptor-1 deficiency protects against streptozotocin-induced diabetic nephropathy in mice.Scientific reports · 2016Article
- Protease activated receptor-1 regulates macrophage-mediated cellular senescence: a risk for idiopathic pulmonary fibrosis.Oncotarget · 2015Article
- A brief exposure to tryptase or thrombin potentiates fibrocyte differentiation in the presence of serum or serum amyloid p.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Trypsin, Tryptase, and Thrombin Polarize Macrophages towards a Pro-Fibrotic M2a Phenotype.PloS one · 2015Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence shows that protease-activated receptor-1 (PAR-1) plays an important role in the development of fibrosis, including lung fibrosis. However, whether PAR-1 also plays a role in the development of skin fibrosis remains elusive. The aim of this study was to determine the role of PAR-1 in the development of skin fibrosis. To explore possible mechanisms by which PAR-1 could play a role, human dermal fibroblasts and keratinocytes were stimulated with specific PAR-1 agonists or antagonists. To investigate the role of PAR-1 in skin fibrosis, we subjected wild-type and PAR-1-deficient mice to a model of bleomycin-induced skin fibrosis. PAR-1 activation leads to increased proliferation and extra cellular matrix (ECM) production, but not migration of human dermal fibroblasts (HDF) in vitro. Moreover, transforming growth factor (TGF)-β production was increased in keratinocytes upon PAR-1 activation, but not in HDF. The loss of PAR-1 in vivo significantly attenuated bleomycin-induced skin fibrosis. The bleomycin-induced increase in dermal thickness and ECM production was reduced significantly in PAR-1-deficient mice compared with wild-type mice. Moreover, TGF-β expression and the number of proliferating fibroblasts were reduced in PAR-1-deficient mice although the difference did not reach statistical significance. This study demonstrates that PAR-1 contributes to the development of skin fibrosis and we suggest that PAR-1 potentiates the fibrotic response mainly by inducing fibroblast proliferation and ECM production.
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