{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T01:30:42Z","timestamp":1788917442980,"version":"build-2803163510"},"reference-count":26,"publisher":"SAGE Publications","license":[{"start":{"date-parts":[[2009,1,1]],"date-time":"2009-01-01T00:00:00Z","timestamp":1230768000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Biomark\ufffdInsights"],"published-print":{"date-parts":[[2009,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Acute aortic dissection (AAD) is a life-threatening condition with high mortality and a relatively unclarified pathophysiological mechanism. Although differentially expressed genes in AAD have been recognized, interactions between these genes remain poorly defined. This study was conducted to gain a better understanding of the molecular mechanisms underlying AAD and to support the future development of a clinical test for monitoring patients at high risk.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and Methods<\/jats:title>\n                    <jats:p>Aortic tissue was collected from 19 patients with AAD (mean age 61.7 \u00b1 13.1 years), and from eight other patients (mean age 32.9 \u00b1 12.2 years) who carried the mutated gene for Marfan syndrome (MS). Six patients (mean age 56.7 \u00b1 12.3 years) served as the control group. The PIQOR\u2122 Immunology microarray with 1076 probes in quadruplicates was utilized; the differentially expressed genes were analysed in a MedScan search using PathwayAssist software. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and protein analysis were performed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Interactions of MS fibrillin-1 (FBN1) in the MedScan pathway analysis showed four genes, fibulin-1 (FBLN1), fibulin-2 (FBLN2), decorin (DCN) and microfibrillar associated protein 5 (MFAP5), which were differentially expressed in all tissue from AAD. The validation of these genes by qRT-PCR revealed a minimum of three-fold downregulation of FBLN1 (0.5 \u00b1 0.4 vs. 6.1 \u00b1 2.3 fold, p = 0.003) and of DCN (2.5 \u00b1 1.0 vs. 8.5 \u00b1 4.7 fold, p = 0.04) in AAD compared to MS and control samples.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Downregulation of fibrillin-1 (FBN1) may weaken extracellular components in the aorta and\/or interfer with the transmission of cellular signals and eventually cause AAD. Additional research on these four identified genes can be a starting point to develop a diagnostic tool.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.4137\/bmi.s2530","type":"journal-article","created":{"date-parts":[[2017,11,7]],"date-time":"2017-11-07T11:43:15Z","timestamp":1510054995000},"page":"BMI.S2530","source":"Crossref","is-referenced-by-count":22,"title":["Pathway Analysis of Differentially Expressed Genes in Patients with Acute Aortic Dissection"],"prefix":"10.4137","volume":"4","author":[{"given":"Salah A.","family":"Mohamed","sequence":"first","affiliation":[{"name":"Department of Cardiac Surgery, University Clinic of Schleswig-Holstein, Campus Luebeck, Luebeck, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hans H.","family":"Sievers","sequence":"additional","affiliation":[{"name":"Department of Cardiac Surgery, University Clinic of Schleswig-Holstein, Campus Luebeck, Luebeck, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thorsten","family":"Hanke","sequence":"additional","affiliation":[{"name":"Department of Cardiac Surgery, University Clinic of Schleswig-Holstein, Campus Luebeck, Luebeck, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Doreen","family":"Richardt","sequence":"additional","affiliation":[{"name":"Department of Cardiac Surgery, University Clinic of Schleswig-Holstein, Campus Luebeck, Luebeck, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claudia","family":"Schmidtke","sequence":"additional","affiliation":[{"name":"Department of Cardiac Surgery, University Clinic of Schleswig-Holstein, Campus Luebeck, Luebeck, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Efstratios I.","family":"Charitos","sequence":"additional","affiliation":[{"name":"Department of Cardiac Surgery, University Clinic of Schleswig-Holstein, Campus Luebeck, Luebeck, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gazanfer","family":"Belge","sequence":"additional","affiliation":[{"name":"Center for Human Genetics, University of Bremen, Bremen, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joern","family":"Bullerdiek","sequence":"additional","affiliation":[{"name":"Center for Human Genetics, University of Bremen, Bremen, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2009,5,6]]},"reference":[{"key":"bibr1-BMI.S2530","first-page":"1422","volume-title":"Heart Disease","author":"Isselbacher 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