{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,18]],"date-time":"2026-07-18T03:53:58Z","timestamp":1784346838949,"version":"3.55.0"},"reference-count":61,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2021,1,20]],"date-time":"2021-01-20T00:00:00Z","timestamp":1611100800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"German Marfan Foundation"},{"DOI":"10.13039\/100010447","name":"German Centre for Cardiovascular Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100010447","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Aims<\/jats:title>\n                  <jats:p>Marfan syndrome is one of the most common inherited disorders of connective tissue caused by fibrillin-1 mutations, characterized by enhanced transcription factor AP-1 DNA binding activity and subsequently abnormally increased expression and activity of matrix-metalloproteinases (MMPs). We aimed to establish a novel adeno-associated virus (AAV)-based strategy for long-term expression of an AP-1 neutralizing RNA hairpin (hp) decoy oligonucleotide (dON) in the aorta to prevent aortic elastolysis in a murine model of Marfan syndrome.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods and results<\/jats:title>\n                  <jats:p>Using fibrillin-1 hypomorphic mice (mgR\/mgR), aortic grafts from young (9\u2009weeks old) donor mgR\/mgR mice were transduced ex vivo with AAV vectors and implanted as infrarenal aortic interposition grafts in mgR\/mgR mice. Grafts were explanted after 30\u2009days. For in vitro studies, isolated primary aortic smooth muscle cells (SMCs) from mgR\/mgR mice were used. Elastica-van-Giesson staining visualized elastolysis, reactive oxygen species (ROS) production was assessed using dihydroethidine staining. RNA F.I.S.H. verified AP-1 hp dON generation in the ex vivo transduced aortic tissue. MMP expression and activity were assessed by western blotting and immunoprecipitation combined with zymography.<\/jats:p>\n                  <jats:p>Transduction resulted in stable therapeutic dON expression in endothelial and SMCs. MMP expression and activity, ROS formation as well as expression of monocyte chemoattractant protein-1 were significantly reduced. Monocyte graft infiltration declined and the integrity of the elastin architecture was maintained. RNAseq analysis confirmed the beneficial effect of AP-1 neutralization on the pro-inflammatory environment in SMCs.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>This novel approach protects from deterioration of aortic stability by sustained delivery of nucleic acids-based therapeutics and further elucidated how to interfere with the mechanism of elastolysis.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/cvr\/cvab012","type":"journal-article","created":{"date-parts":[[2021,1,13]],"date-time":"2021-01-13T17:37:41Z","timestamp":1610559461000},"page":"2459-2473","source":"Crossref","is-referenced-by-count":19,"title":["AAV-mediated AP-1 decoy oligonucleotide expression inhibits aortic elastolysis in a mouse model of Marfan syndrome"],"prefix":"10.1093","volume":"117","author":[{"given":"Anca","family":"Remes","sequence":"first","affiliation":[{"name":"Department of Internal Medicine III, University of Kiel, University Hospital Schleswig-Holstein , Kiel, Germany"},{"name":"German Centre for Cardiovascular Research, Partner Site Hamburg\/Kiel\/L\u00fcbeck , Kiel, Germany"},{"name":"Division of Cardiovascular Physiology, Institute of Physiology and Pathophysiology, Heidelberg University , Im Neuenheimer Feld 326, 69120 Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rawa","family":"Arif","sequence":"additional","affiliation":[{"name":"Department of Cardiac Surgery, University Hospital Heidelberg , Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maximilian","family":"Franz","sequence":"additional","affiliation":[{"name":"Department of Cardiac Surgery, University Hospital Heidelberg , Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas","family":"Jungmann","sequence":"additional","affiliation":[{"name":"Internal Medicine III, University Hospital 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Luxembourg"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Markus","family":"Hecker","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Physiology, Institute of Physiology and Pathophysiology, Heidelberg University , Im Neuenheimer Feld 326, 69120 Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8223-2638","authenticated-orcid":false,"given":"Oliver J","family":"M\u00fcller","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine III, University of Kiel, University Hospital Schleswig-Holstein , Kiel, Germany"},{"name":"German Centre for Cardiovascular Research, Partner Site Hamburg\/Kiel\/L\u00fcbeck , Kiel, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2723-5953","authenticated-orcid":false,"given":"Andreas H","family":"Wagner","sequence":"additional","affiliation":[{"name":"Division of 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