ArticleLaboratory investigation; a journal of technical methods and pathology2014
Increased expression of protease nexin-1 in fibroblasts during idiopathic pulmonary fibrosis regulates thrombin activity and fibronectin expression.
Article in Laboratory investigation; a journal of technical methods and pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- IFN-γ could induce ferroptosis in keloid fibroblasts by inhibiting the expression of serpine2.Cell death discovery · 2025Article
- Emergence of inflammatory fibroblasts with aging in Hermansky-Pudlak syndrome associated pulmonary fibrosis.Communications biology · 2025Article
- Epigenetic modification regulates the ligamentum flavum hypertrophy through miR-335-3p/SERPINE2/β-catenin signaling pathway.Cellular & molecular biology letters · 2025Article
- Identification of Fibroinflammatory and Fibrotic Transcriptomic Subsets of Human Cutaneous Sclerotic Chronic Graft-Versus-Host Disease.JID innovations : skin science from molecules to population health · 2024Article
- DNA accelerates the protease inhibition of a bacterial serpin chloropin.Frontiers in molecular biosciences · 2023Article
- Comparative proteome analysis of the ligamentum flavum of patients with lumbar spinal canal stenosis.JOR spine · 2022Article
- Endocytosis of Peptidase Inhibitor SerpinE2 promotes Myocardial Fibrosis through activating ERK1/2 and β-catenin Signaling Pathways.International journal of biological sciences · 2022Article
- Protease nexin-1 deficiency increases mouse hindlimb neovascularisation following ischemia and accelerates femoral artery perfusion.Scientific reports · 2021Article
- Therapeutic SERPINs: Improving on Nature.Frontiers in cardiovascular medicine · 2021Review
- Protease Nexin-1 in the Cardiovascular System: Wherefore Art Thou?Frontiers in cardiovascular medicine · 2021Review
- Hematopoietic protease nexin-1 protects against lung injury by preventing thrombin signaling in mice.Blood advances · 2018Article
- ZEB1-repressed microRNAs inhibit autocrine signaling that promotes vascular mimicry of breast cancer cells.Oncogene · 2018Article
- The involvement of the laminin-integrin α7β1 signaling pathway in mechanical ventilation-induced pulmonary fibrosis.Journal of thoracic disease · 2017Article
- Comparison of two neurotrophic serpins reveals a small fragment with cell survival activity.Molecular vision · 2017Article
- Inhibition of SERPINE2/protease nexin-1 by a monoclonal antibody attenuates airway remodeling in a murine model of asthma.International journal of clinical and experimental pathology · 2017Article
- Overexpression of SerpinE2/protease nexin-1 Contribute to Pathological Cardiac Fibrosis via increasing Collagen Deposition.Scientific reports · 2016Article
- High temperature requirement A1 and fibronectin: two possible players in placental tissue remodelling.European journal of histochemistry : EJH · 2016Article
- The Involvement of Protease Nexin-1 (PN1) in the Pathogenesis of Intervertebral Disc (IVD) Degeneration.Scientific reports · 2016Article
- Serpine2 deficiency results in lung lymphocyte accumulation and bronchus-associated lymphoid tissue formation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic diffuse lung disease characterized by an accumulation of excess fibrous material in the lung. Protease nexin-1 (PN-1) is a tissue serpin produced by many cell types, including lung fibroblasts. PN-1 is capable of regulating proteases of both coagulation and fibrinolysis systems, by inhibiting, respectively, thrombin and plasminergic enzymes. PN-1 is thus a good candidate for regulating tissue remodeling occurring during IPF. We demonstrated a significant increase of PN-1 expression in lung tissue extracts, lung fibroblasts and bronchoalveolar lavage fluids of patients with IPF. The increase of PN-1 expression was reproduced after stimulation of control lung fibroblasts by transforming growth factor-β, a major pro-fibrotic cytokine involved in IPF. Another serpin, plasminogen activator inhibitor-1 (PAI-1) is also overexpressed in fibrotic fibroblasts. Unlike PAI-1, cell-bound PN-1 as well as secreted PN-1 from IPF and stimulated fibroblasts were shown to inhibit efficiently thrombin activity, indicating that both serpins should exhibit complementary roles in IPF pathogenesis, via their different preferential antiprotease activities. Moreover, we observed that overexpression of PN-1 induced by transfection of control fibroblasts led to increased fibronectin expression, whereas PN-1 silencing induced in fibrotic fibroblasts led to decreased fibronectin expression. Overexpression of PN-1 lacking either its antiprotease activity or its binding capacity to glycosaminoglycans had no effect on fibronectin expression. These novel findings suggest that modulation of PN-1 expression in lung fibroblasts may also have a role in the development of IPF by directly influencing the expression of extracellular matrix proteins. Our data provide new insights into the role of PN-1 in the poorly understood pathological processes involved in IPF and could therefore give rise to new therapeutic approaches.
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