{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T14:54:50Z","timestamp":1778856890091,"version":"3.51.4"},"reference-count":43,"publisher":"Springer Science and Business Media LLC","issue":"1","license":[{"start":{"date-parts":[[2015,2,4]],"date-time":"2015-02-04T00:00:00Z","timestamp":1423008000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2015,2,4]],"date-time":"2015-02-04T00:00:00Z","timestamp":1423008000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Arthritis Res Ther"],"abstract":"<jats:title>Abstract<\/jats:title><jats:sec>\n                        <jats:title>Introduction<\/jats:title>\n                        <jats:p>The link between cardiovascular disease (CVD) and patients with chronic inflammation is not clearly understood. We examined a knock-in mouse expressing a poly-ubiquitin-binding-defective mutant of the protein ABIN1 (ABIN1(D485N)), which develops a systemic lupus erythematosus-like autoimmune disease because of the hyperactivation of I\u03baB kinases (I\u03baKs) and mitogen-activated protein kinases (MAPKs). These mice were used to determine the potential role of these signaling pathways in inflammation-mediated CVD development.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Methods<\/jats:title>\n                        <jats:p>Laser Doppler imaging in combination with the iontophoresis of vasoactive chemicals were used to assess endothelium-dependent vasodilatation <jats:italic>in vivo<\/jats:italic> in ABIN1 (D485N)) mutant defective (<jats:italic>n<\/jats:italic>\u2009=\u200929) and wild-type (WT) control (<jats:italic>n<\/jats:italic>\u2009=\u200926) mice. Measurements were made at baseline, and animals were subdivided to receive either chow or a proatherogenic diet for 4\u00a0weeks, after which, follow-up assessments were made. Paired and unpaired <jats:italic>t<\/jats:italic> tests, and ANOVA with <jats:italic>post hoc<\/jats:italic> Bonferroni correction were used for statistical significance at <jats:italic>P<\/jats:italic> &lt;0.05.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Results<\/jats:title>\n                        <jats:p>Endothelium-dependent vasodilatation to acetylcholine was attenuated at 4\u00a0weeks in ABIN1(D485N)-chow-fed mice compared with age-matched WT-chow-fed mice (<jats:italic>P<\/jats:italic> &lt;0.05). The magnitude of attenuation was similar to that observed in WT-cholesterol-fed animals (versus WT-chow, <jats:italic>P<\/jats:italic> &lt;0.01). ABIN1(D485N)-cholesterol-fed mice had the poorest endothelium-dependent responses compared with other groups (<jats:italic>P<\/jats:italic> &lt;0.001). ABIN1(D485N)-chow-fed mice had increased plasma interleukin-6 (IL-6) levels (versus WT-chow, <jats:italic>P<\/jats:italic> &lt;0.001), and this was further elevated in ABIN1(D485N)-cholesterol-fed mice (versus ABIN1(D485N)-chow; <jats:italic>P<\/jats:italic> &lt;0.05). IL-1\u03b1 was significantly greater in all groups compared with WT-chow (<jats:italic>P<\/jats:italic> &lt;0.01). ABIN1(D485N) mice showed significant cardiac hypertrophy (<jats:italic>P<\/jats:italic> &lt;0.05).<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Conclusions<\/jats:title>\n                        <jats:p>The ABIN(D485N) mice display endothelial dysfunction and cardiac hypertrophy, which is possibly mediated through IL-6 and, to a lesser degree, IL-1\u03b1. These results suggest that the ABIN1-mediated hyperactivation of IKKs and MAPKs might mediate chronic inflammation and CVD development.<\/jats:p>\n                     <\/jats:sec>","DOI":"10.1186\/s13075-015-0543-3","type":"journal-article","created":{"date-parts":[[2015,2,3]],"date-time":"2015-02-03T16:25:49Z","timestamp":1422980749000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["An important role for A20-binding inhibitor of nuclear factor-kB-1 (ABIN1) in inflammation-mediated endothelial dysfunction: an in vivo study in ABIN1 (D485N) mice"],"prefix":"10.1186","volume":"17","author":[{"given":"Naveed","family":"Akbar","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sambit","family":"Nanda","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jill","family":"Belch","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Philip","family":"Cohen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Faisel","family":"Khan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2015,2,4]]},"reference":[{"key":"543_CR1","doi-asserted-by":"publisher","first-page":"607084","DOI":"10.1155\/2010\/607084","volume":"2010","author":"C Lopez-Pedrera","year":"2010","unstructured":"Lopez-Pedrera C, Aguirre MA, Barbarroja N, Cuadrado MJ. 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