Immune system-mediated atherosclerosis caused by deficiency of long non-coding RNA MALAT1 in ApoE−/−mice

Abstract Aims The immune system is considered a key driver of atherosclerosis, and beyond proteins and microRNAs (miRs), long non-coding RNAs (lncRNAs) are implicated in immune control. We previously described that lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in...

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Veröffentlicht in:Cardiovascular research 2019-02, Vol.115 (2), p.302-314
Hauptverfasser: Gast, Martina, Rauch, Bernhard H, Nakagawa, Shinichi, Haghikia, Arash, Jasina, Andrzej, Haas, Jan, Nath, Neetika, Jensen, Lars, Stroux, Andrea, Böhm, Andreas, Friebel, Julian, Rauch, Ursula, Skurk, Carsten, Blankenberg, Stefan, Zeller, Tanja, Prasanth, Kannanganattu V, Meder, Benjamin, Kuss, Andreas, Landmesser, Ulf, Poller, Wolfgang
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Sprache:eng
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Zusammenfassung:Abstract Aims The immune system is considered a key driver of atherosclerosis, and beyond proteins and microRNAs (miRs), long non-coding RNAs (lncRNAs) are implicated in immune control. We previously described that lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in cardiac innate immunity in a myocarditis model. Here, we investigated the impact of MALAT1 deficiency upon atherosclerosis development. Methods and results Heterozygous MALAT1-deficient ApoE−/− mice displayed massive immune system dysregulation and atherosclerosis within 2 months even when kept on normal diet. Aortic plaque area (P 
ISSN:0008-6363
1755-3245
DOI:10.1093/cvr/cvy202