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 |
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Hauptverfasser: | , , , , , , , , , , , , , , , , , , , |
Format: | Artikel |
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 |
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ISSN: | 0008-6363 1755-3245 |
DOI: | 10.1093/cvr/cvy202 |