{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T16:26:02Z","timestamp":1787502362446,"version":"build-2736575974"},"reference-count":56,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2010,9,1]],"date-time":"2010-09-01T00:00:00Z","timestamp":1283299200000},"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":[[2010,9,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Rationale<\/jats:title>\n                    <jats:p>Idiopathic pulmonary arterial hypertension (IPAH) is characterized by medial hypertrophy due to pulmonary artery smooth muscle cell (paSMC) hyperplasia. Inflammation is proposed to play a role in vessel remodeling associated with IPAH. IL-13 is emerging as a regulator of tissue remodeling; however, the contribution of the IL-13 system to IPAH has not been assessed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>The objective of this study was to assess the possible contribution of the IL-13 system to IPAH.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Expression and localization of IL-13, and IL-13 receptors IL-4R, IL-13R\u03b11, and IL-13R\u03b12 were assessed by real-time reverse transcription\u2013polymerase chain reaction, immunohistochemistry, and flow cytometry in lung tissue, paSMC, and microdissected vascular lesions from patients with IPAH, and in lung tissue from rodents with hypoxia- or monocrotaline-induced pulmonary hypertension. A whole-genome microarray analysis was used to study IL-13\u2013regulated genes in paSMC.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>Pulmonary expression of the IL-13 decoy receptor IL-13R\u03b12 was up-regulated relative to that of the IL-13 signaling receptors IL-4R and IL-13R\u03b11 in patients with IPAH and in two animal models of IPAH. IL-13, signaling via STAT3 and STAT6, suppressed proliferation of paSMC by promoting G0\/G1 arrest. Whole-genome microarrays revealed that IL-13 suppressed endothelin-1 production by paSMC, suggesting that IL-13 controlled paSMC growth by regulating endothelin production. Ectopic expression of the il13ra2 gene resulted in partial loss of paSMC growth control by IL-13 and blunted IL-13 suppression of endothelin-1 production by paSMC, whereas small-interfering RNA knockdown of il13ra2 gene expression had the opposite effects.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The IL-13 system is a novel regulator of paSMC growth. Dysregulation of IL-13 receptor expression in IPAH may partially underlie smooth muscle hypertrophy associated with pathological vascular remodeling in IPAH.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.200909-1367oc","type":"journal-article","created":{"date-parts":[[2010,6,3]],"date-time":"2010-06-03T23:01:26Z","timestamp":1275606086000},"page":"805-818","source":"Crossref","is-referenced-by-count":59,"title":["Dysregulation of the IL-13 Receptor System. A Novel Pathomechanism in Pulmonary Arterial Hypertension"],"prefix":"10.1093","volume":"182","author":[{"given":"Matthias","family":"Hecker","sequence":"first","affiliation":[{"name":"Department of Internal Medicine (Pulmonology)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zbigniew","family":"Zas\u0142ona","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine (Pulmonology)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gra\u017cyna","family":"Kwapiszewska","sequence":"additional","affiliation":[{"name":"Department of Pathology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gero","family":"Niess","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine (Pulmonology)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna","family":"Zakrzewicz","sequence":"additional","affiliation":[{"name":"Department of Experimental Surgery, 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