{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,21]],"date-time":"2026-03-21T07:24:06Z","timestamp":1774077846203,"version":"3.50.1"},"reference-count":54,"publisher":"Oxford University Press (OUP)","issue":"8","license":[{"start":{"date-parts":[[2016,4,1]],"date-time":"2016-04-01T00:00:00Z","timestamp":1459468800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/501100002915","name":"Fondation pour la Recherche Medicale","doi-asserted-by":"crossref","award":["AJE201121"],"award-info":[{"award-number":["AJE201121"]}],"id":[{"id":"10.13039\/501100002915","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Agence Nationale pour la Recherche","award":["ANR-14-CE15-0010-01"],"award-info":[{"award-number":["ANR-14-CE15-0010-01"]}]},{"DOI":"10.13039\/501100015084","name":"Dutch Lung Foundation","doi-asserted-by":"publisher","award":["9.2.14.085FE"],"award-info":[{"award-number":["9.2.14.085FE"]}],"id":[{"id":"10.13039\/501100015084","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000925","name":"National Health and Medical Research Council","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Research Fellowship","award":["1027369"],"award-info":[{"award-number":["1027369"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2016,4,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Rationale<\/jats:title>\n                    <jats:p>Idiopathic pulmonary fibrosis (IPF) is a devastating disease that remains refractory to current therapies.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To characterize the expression and activity of the membrane-anchored serine protease matriptase in IPF in humans and unravel its potential role in human and experimental pulmonary fibrogenesis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Matriptase expression was assessed in tissue specimens from patients with IPF versus control subjects using quantitative reverse transcriptase\u2013polymerase chain reaction, immunohistochemistry, and Western blotting, while matriptase activity was monitored by fluorogenic substrate cleavage. Matriptase-induced fibroproliferative responses and the receptor involved were characterized in human primary pulmonary fibroblasts by Western blot, viability, and migration assays. In the murine model of bleomycin-induced pulmonary fibrosis, the consequences of matriptase depletion, either by using the pharmacological inhibitor camostat mesilate (CM), or by genetic down-regulation using matriptase hypomorphic mice, were characterized by quantification of secreted collagen and immunostainings.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>Matriptase expression and activity were up-regulated in IPF and bleomycin-induced pulmonary fibrosis. In cultured human pulmonary fibroblasts, matriptase expression was significantly induced by transforming growth factor-\u03b2. Furthermore, matriptase elicited signaling via protease-activated receptor-2 (PAR-2), and promoted fibroblast activation, proliferation, and migration. In the experimental bleomycin model, matriptase depletion, by the pharmacological inhibitor CM or by genetic down-regulation, diminished lung injury, collagen production, and transforming growth factor-\u03b2 expression and signaling.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These results implicate increased matriptase expression and activity in the pathogenesis of pulmonary fibrosis in human IPF and in an experimental mouse model. Overall, targeting matriptase, or treatment by CM, which is already in clinical use for other diseases, may represent potential therapies for IPF.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.201502-0299oc","type":"journal-article","created":{"date-parts":[[2015,11,24]],"date-time":"2015-11-24T16:29:14Z","timestamp":1448382554000},"page":"847-860","source":"Crossref","is-referenced-by-count":46,"title":["Membrane-anchored Serine Protease Matriptase Is a Trigger of Pulmonary Fibrogenesis"],"prefix":"10.1093","volume":"193","author":[{"given":"Olivier","family":"Bardou","sequence":"first","affiliation":[{"name":"Inserm UMR1152, Medical School Xavier Bichat, Paris, France"},{"name":"Universit\u00e9 Paris Diderot, Sorbonne Paris Cit\u00e9, D\u00e9partement Hospitalo-universitaire FIRE (Fibrosis, Inflammation and Remodeling) and LabEx Inflamex, Paris, France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Awen","family":"Menou","sequence":"additional","affiliation":[{"name":"Inserm UMR1152, Medical School Xavier Bichat, Paris, France"},{"name":"Universit\u00e9 Paris Diderot, Sorbonne Paris Cit\u00e9, D\u00e9partement Hospitalo-universitaire FIRE (Fibrosis, Inflammation and Remodeling) and LabEx Inflamex, Paris, France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Charl\u00e8ne","family":"Fran\u00e7ois","sequence":"additional","affiliation":[{"name":"Inserm UMR1152, Medical School Xavier Bichat, Paris, France"},{"name":"Universit\u00e9 Paris Diderot, Sorbonne Paris Cit\u00e9, D\u00e9partement Hospitalo-universitaire FIRE (Fibrosis, Inflammation and Remodeling) and LabEx Inflamex, Paris, France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jan Willem","family":"Duitman","sequence":"additional","affiliation":[{"name":"Center for Experimental and Molecular Medicine, Academic Medical Center, Amsterdam, the Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jan H.","family":"von der Th\u00fcsen","sequence":"additional","affiliation":[{"name":"Department of Pathology, Erasmus Medical Centre, Rotterdam, the Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rapha\u00ebl","family":"Borie","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Paris Diderot, Sorbonne Paris Cit\u00e9, D\u00e9partement Hospitalo-universitaire FIRE (Fibrosis, Inflammation and Remodeling) and LabEx Inflamex, Paris, France"},{"name":"Assistance Publique-H\u00f4pitaux de Paris, Department of Pulmonology A, Competence Center for Rare Lung Diseases, Bichat-Claude Bernard University Hospital, Paris, France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Katiuchia Uzzun","family":"Sales","sequence":"additional","affiliation":[{"name":"Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland"},{"name":"Department of Cell and Molecular Biology, Ribeir\u00e3o Preto School of Medicine, University of S\u00e3o Paulo Ribeir\u00e3o Preto, S\u00e3o Paulo, Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kathrin","family":"Mutze","sequence":"additional","affiliation":[{"name":"Member of the German Center of Lung Research, Comprehensive Pneumology Center, University Hospital, Ludwig-Maximilians University, Helmholtz Zentrum M\u00fcnchen, Munich, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yves","family":"Castier","sequence":"additional","affiliation":[{"name":"Assistance Publique-H\u00f4pitaux de Paris, Department of Vascular and Thoracic Surgery, Bichat-Claude Bernard University Hospital, Denis Diderot University and Medical School Paris VII, 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