{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,11]],"date-time":"2026-10-11T21:33:29Z","timestamp":1791754409214,"version":"4.3.4"},"reference-count":51,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2022,3,1]],"date-time":"2022-03-01T00:00:00Z","timestamp":1646092800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/501100000031","name":"Canadian Institutes of Health Research Institute of Human Development, Child and Youth Health","doi-asserted-by":"crossref","award":["FRN162226"],"award-info":[{"award-number":["FRN162226"]}],"id":[{"id":"10.13039\/501100000031","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Canada Foundation for Innovation John R. 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Evans Leaders Fund","doi-asserted-by":"publisher","award":["37315"],"award-info":[{"award-number":["37315"]}],"id":[{"id":"10.13039\/501100000196","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.atsjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2022,3,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Rationale<\/jats:title>\n                    <jats:p>Extremely preterm infants develop bronchopulmonary dysplasia (BPD), a chronic lung injury that lacks effective treatment. TSP-1 (thrombospondin-1) is an antiangiogenic protein that activates TGF-\u03b21 (transforming growth factor-\u03b21), a cytokine strongly linked to both experimental and human BPD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>1) To examine effects of inhibiting TSP-1\u2013mediated TGF-\u03b21 activation (LSKL [leucine\u2013serine\u2013lysine\u2013leucine]) in neonatal rats with bleomycin-induced lung injury; 2) to examine effects of a TSP-1 mimic (ABT-510) on lung morphology; and 3) to determine whether TSP-1 and related signaling peptides are increased in lungs of human preterm infants at risk for BPD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>From Postnatal Days 1 to 14, rat pups received daily intraperitoneal bleomycin (1 mg\/kg) or vehicle and were treated with daily subcutaneous LSKL (20 mg\/kg) or vehicle alone. Separate animals were treated with vehicle or ABT-510 (30 mg\/kg\/d). Paraffin-embedded lung tissues from 47 autopsies (controls; death &amp;lt;28 d, n\u2009=\u200930 and BPD at risk; death \u2a7e28 d, n\u2009=\u200917) performed on infants born &amp;lt;29 completed weeks\u2019 gestation were semiquantified for injury markers (collagen, macrophages, and 3-nitrotyrosine), TSP-1, and TGF-\u03b21.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>Bleomycin or ABT-510 increased lung TGF-\u03b21 activity and macrophage influx, caused pulmonary hypertension, and led to alveolar and microvascular hypoplasia. Treatment with LSKL partially prevented abnormal lung morphology secondary to bleomycin. Lungs from human infants at risk for BPD had increased contents of TSP-1 and TGF-\u03b21 when compared with controls. TGF-\u03b21 content correlated with markers of lung injury.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>TSP-1 inhibits alveologenesis in neonatal rats, in part via the upregulated activity of TGF-\u03b21. Observations in human lungs suggest a similar pathogenic role for TSP-1 in infants at risk for BPD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.202104-1021oc","type":"journal-article","created":{"date-parts":[[2022,1,12]],"date-time":"2022-01-12T18:24:25Z","timestamp":1642011865000},"page":"685-699","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":24,"title":["Thrombospondin-1 Plays a Major Pathogenic Role in Experimental and Human Bronchopulmonary Dysplasia"],"prefix":"10.1093","volume":"205","author":[{"given":"Brittany Ann","family":"Ruschkowski","sequence":"first","affiliation":[{"name":"Molecular Biomedicine Program, Children\u2019s Hospital of Eastern Ontario Research Institute, Ottawa, Ontario, Canada; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yousef","family":"Esmaeil","sequence":"additional","affiliation":[{"name":"Department of Paediatrics and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kate","family":"Daniel","sequence":"additional","affiliation":[{"name":"Molecular Biomedicine Program, Children\u2019s Hospital of Eastern Ontario Research Institute, Ottawa, Ontario, Canada; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chantal","family":"Gaudet","sequence":"additional","affiliation":[{"name":"Molecular Biomedicine Program, Children\u2019s Hospital of Eastern Ontario Research Institute, Ottawa, Ontario, Canada; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Behzad","family":"Yeganeh","sequence":"additional","affiliation":[{"name":"Molecular Biomedicine Program, Children\u2019s Hospital of Eastern Ontario Research Institute, Ottawa, Ontario, Canada; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Grynspan","sequence":"additional","affiliation":[{"name":"Department of Paediatrics 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