{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T07:43:15Z","timestamp":1791186195512,"version":"4.1.0"},"reference-count":49,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2012,10,1]],"date-time":"2012-10-01T00:00:00Z","timestamp":1349049600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2012,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Rationale<\/jats:title>\n                    <jats:p>Pulmonary arterial hypertension (PAH) is a progressive and fatal disease characterized by pulmonary arterial muscularization due to excessive pulmonary vascular cell proliferation and migration, a phenotype dependent upon growth factors and activation of receptor tyrosine kinases (RTKs). p130Cas is an adaptor protein involved in several cellular signaling pathways that control cell migration, proliferation, and survival.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>We hypothesized that in experimental and human PAH p130Cas signaling is overactivated, thereby facilitating the intracellular transmission of signal induced by fibroblast growth factor (FGF)2, epidermal growth factor (EGF), and platelet-derived growth factor (PDGF).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>In patients with PAH, levels of p130Cas protein and\/or activity are higher in the serum, in the walls of distal pulmonary arteries, in cultured smooth muscle cells (PA-SMCs), and in pulmonary endothelial cells (P-ECs) than in control subjects. These abnormalities in the p130Cas signaling were also found in the chronically hypoxic mice and monocrotaline-injected rats as models of human PAH. We obtained evidence for the convergence and amplification of the growth-stimulating effect of the EGF-, FGF2-, and PDGF-signaling pathways via the p130Cas signaling pathway. We found that daily treatment with the EGF-R inhibitor gefitinib, the FGF-R inhibitor dovitinib, and the PDGF-R inhibitor imatinib started 2 weeks after a subcutaneous monocrotaline injection substantially attenuated the abnormal increase in p130Cas and ERK1\/2 activation and regressed established pulmonary hypertension.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our findings demonstrate that p130Cas signaling plays a critical role in experimental and idiopathic PAH by modulating pulmonary vascular cell migration and proliferation and by acting as an amplifier of RTK downstream signals.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.201202-0309oc","type":"journal-article","created":{"date-parts":[[2012,7,14]],"date-time":"2012-07-14T05:30:50Z","timestamp":1342243850000},"page":"666-676","source":"Crossref","is-referenced-by-count":95,"title":["A Critical Role for p130Cas in the Progression of Pulmonary Hypertension in Humans and Rodents"],"prefix":"10.1093","volume":"186","author":[{"given":"Ly","family":"Tu","sequence":"first","affiliation":[{"name":"INSERM UMR 999, LabEx LERMIT, Centre Chirurgical Marie Lannelongue, Le Plessis-Robinson, France"},{"name":"Universit\u00e9 Paris-Sud, School of Medicine, Kremlin-Bic\u00eatre, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frances S.","family":"De Man","sequence":"additional","affiliation":[{"name":"INSERM UMR 999, LabEx LERMIT, Centre Chirurgical Marie Lannelongue, Le Plessis-Robinson, France"},{"name":"Universit\u00e9 Paris-Sud, School of Medicine, Kremlin-Bic\u00eatre, France"},{"name":"VU University Medical Center, Amsterdam, The Netherlands; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Barbara","family":"Girerd","sequence":"additional","affiliation":[{"name":"INSERM UMR 999, LabEx LERMIT, Centre Chirurgical Marie Lannelongue, Le 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