{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T01:15:09Z","timestamp":1789521309767,"version":"build-2803163510"},"reference-count":44,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2018,10,18]],"date-time":"2018-10-18T00:00:00Z","timestamp":1539820800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["8177021278"],"award-info":[{"award-number":["8177021278"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2018,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>The reversibility of pulmonary arterial hypertension (<jats:styled-content style=\"fixed-case\">PAH<\/jats:styled-content>) in congenital heart disease (<jats:styled-content style=\"fixed-case\">CHD<\/jats:styled-content>) is of great importance for the operability of <jats:styled-content style=\"fixed-case\">CHD<\/jats:styled-content>. Proteomics analysis found that transgelin was significantly up\u2010regulated in the lung tissue of <jats:styled-content style=\"fixed-case\">CHD<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PAH<\/jats:styled-content> patients, especially in the irreversible group. However, how exactly it participated in <jats:styled-content style=\"fixed-case\">CHD<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PAH<\/jats:styled-content> development is unknown.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Immunohistochemical staining and Western blot were performed for further qualitative and quantitative analysis of transgelin in the lung tissues of <jats:styled-content style=\"fixed-case\">CHD<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PAH<\/jats:styled-content> patients. The mechanism of transgelin in <jats:styled-content style=\"fixed-case\">CHD<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PAH<\/jats:styled-content> development was explored in\u00a0vitro. Primary human pulmonary arterial smooth muscle cells (hPASMCs) were cultured and infected with TAGLN siRNA or TAGLN lentiviral vector. Cell morphologic change (Coomassie Brilliant Blue staining), proliferation (cell count and EdU assay), apoptosis (terminal deoxyribonucleotidyl transferase mediated dUTP nick end labeling assay and Annexin\u2010V flow cytometry) and migration (transwell) were evaluated following the cell treatment. The <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> and protein expression levels were detected in real\u2010time <jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content> and Western blot.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In line with the proteomic findings, transgelin was obviously expressed in <jats:styled-content style=\"fixed-case\">PASMC<\/jats:styled-content> of the middle pulmonary arterioles, especially in the irreversible <jats:styled-content style=\"fixed-case\">PAH<\/jats:styled-content> group. Also, transgelin expression showed positive relation with pathological grading. Experiment in\u00a0vitro demonstrated that transgelin overexpression promoted <jats:styled-content style=\"fixed-case\">PASMC<\/jats:styled-content> proliferation and migration, strengthened cytoskeleton and was accompanied by increased expression of synthetic phenotype markers (osteopontin, proliferating cell nuclear antigen) and anti\u2010apoptotic protein (bcl\u20102). On the other hand, suppression of transgelin expression activated <jats:styled-content style=\"fixed-case\">PASMC<\/jats:styled-content> apoptosis, reducing cell proliferation and migration.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Transgelin may be a potential target in the development of irreversible <jats:styled-content style=\"fixed-case\">CHD<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PAH<\/jats:styled-content> through inducing <jats:styled-content style=\"fixed-case\">PASMC<\/jats:styled-content> phenotype change, proliferation, migration and reducing cell apoptosis.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jcmm.13912","type":"journal-article","created":{"date-parts":[[2018,10,19]],"date-time":"2018-10-19T04:09:56Z","timestamp":1539922196000},"page":"6249-6261","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["Transgelin as a potential target in the 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Pulmonary Vascular Disease State Key Laboratory of Cardiovascular Disease Fuwai Hospital National Center for Cardiovascular Diseases Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wen","family":"Li","sequence":"additional","affiliation":[{"name":"Center of Pulmonary Vascular Disease State Key Laboratory of Cardiovascular Disease Fuwai Hospital National Center for Cardiovascular Diseases Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"Song","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Cardiovascular Disease Fuwai Hospital National Center for Cardiovascular Diseases Chinese Academy of Medical Sciences and Peking Union Medical College Beijing 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