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Increased abundance of\n                    <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>\n                    1 is associated with several pathological disorders such as cancer, asthma and chronic obstructive pulmonary disease (\n                    <jats:styled-content style=\"fixed-case\">COPD<\/jats:styled-content>\n                    ). In this study, we investigated the relevance of\n                    <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>\n                    1 in the pathological remodelling present in patients with idiopathic pulmonary arterial hypertension (\n                    <jats:styled-content style=\"fixed-case\">IPAH<\/jats:styled-content>\n                    ) and pulmonary hypertension (\n                    <jats:styled-content style=\"fixed-case\">PH<\/jats:styled-content>\n                    ) associated with\n                    <jats:styled-content style=\"fixed-case\">COPD<\/jats:styled-content>\n                    . Remodelled vessels present in\n                    <jats:styled-content style=\"fixed-case\">COPD<\/jats:styled-content>\n                    with\n                    <jats:styled-content style=\"fixed-case\">PH<\/jats:styled-content>\n                    and\n                    <jats:styled-content style=\"fixed-case\">IPAH<\/jats:styled-content>\n                    lung samples were often surrounded by\n                    <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>\n                    1\u2010positive cells. Increased\n                    <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>\n                    1 serum levels were detected in both patient populations compared to control samples. The effects of physiological\n                    <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>\n                    1 concentrations were then examined on cellular responses\n                    <jats:italic>in vitro<\/jats:italic>\n                    .\n                    <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>\n                    1 enhanced proliferation of pulmonary arterial smooth muscle cells (\n                    <jats:styled-content style=\"fixed-case\">PASMC<\/jats:styled-content>\n                    ) and primary human arterial endothelial cells (\n                    <jats:styled-content style=\"fixed-case\">PAEC<\/jats:styled-content>\n                    ).\n                    <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>\n                    1 stimulated p38, extracellular signal\u2010regulated kinase (\n                    <jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>\n                    ) and c\u2010Jun N\u2010terminal kinase (\n                    <jats:styled-content style=\"fixed-case\">JNK<\/jats:styled-content>\n                    ) phosphorylation. Furthermore, activation of the downstream\n                    <jats:styled-content style=\"fixed-case\">AP<\/jats:styled-content>\n                    \u20101 complex proteins c\u2010Fos and c\u2010Jun was observed. Silencing of c\u2010Jun ablated the\n                    <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>\n                    1\u2010induced proliferation in\n                    <jats:styled-content style=\"fixed-case\">PASMC<\/jats:styled-content>\n                    . Thus, an inflammatory component such as\n                    <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>\n                    1 can contribute to\n                    <jats:styled-content style=\"fixed-case\">PASMC<\/jats:styled-content>\n                    and\n                    <jats:styled-content style=\"fixed-case\">PAEC<\/jats:styled-content>\n                    proliferation and therefore potentially to vascular remodelling and\n                    <jats:styled-content style=\"fixed-case\">PH<\/jats:styled-content>\n                    pathogenesis.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.12519","type":"journal-article","created":{"date-parts":[[2015,2,28]],"date-time":"2015-02-28T00:27:52Z","timestamp":1425083272000},"page":"1151-1161","source":"Crossref","is-referenced-by-count":55,"title":["High\u2010mobility group box\u20101 induces vascular remodelling processes\n                    <i>via<\/i>\n                    c\u2010Jun activation"],"prefix":"10.1111","volume":"19","author":[{"given":"Diana","family":"Zabini","sequence":"first","affiliation":[{"name":"Ludwig Boltzmann Institute for Lung Vascular Research Graz Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Slaven","family":"Crnkovic","sequence":"additional","affiliation":[{"name":"Ludwig Boltzmann Institute for Lung Vascular Research Graz Austria"},{"name":"Experimental Anaesthesiology Department of Anaesthesia and Intensive Care Medicine Medical University of Graz Graz Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hui","family":"Xu","sequence":"additional","affiliation":[{"name":"Experimental Anaesthesiology Department of Anaesthesia and Intensive Care Medicine Medical University of Graz Graz Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria","family":"Tscherner","sequence":"additional","affiliation":[{"name":"Ludwig Boltzmann Institute for Lung Vascular Research Graz 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