Long Non-Coding RNA Malat-1 Is Dispensable during Pressure Overload-Induced Cardiac Remodeling and Failure in Mice

Tim Peters, Steffie Beijnsberger, Abdelaziz Beqqali, Nicole Bitsch, Shinichi Nakagawa, Kannanganattu V. Prasanth, Leon J. de Windt, Ralph J. van Oort, Stephane Heymans, Blanche Schroen*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

35 Citations (Web of Science)

Abstract

Background Long non-coding RNAs (lncRNAs) are a class of RNA molecules with diverse regulatory functions during embryonic development, normal life, and disease in higher organisms. However, research on the role of lncRNAs in cardiovascular diseases and in particular heart failure is still in its infancy. The exceptionally well conserved nuclear lncRNA Metastasis associated in lung adenocarcinoma transcript 1 (Malat-1) is a regulator of mRNA splicing and highly expressed in the heart. Malat-1 modulates hypoxia-induced vessel growth, activates ERK/MAPK signaling, and scavenges the anti-hypertrophic microRNA-133. We therefore hypothesized that Malat-1 may act as regulator of cardiac hypertrophy and failure during cardiac pressure overload induced by thoracic aortic constriction (TAC) in mice. Results Absence of Malat-1 did not affect cardiac hypertrophy upon pressure overload: Heart weight to tibia length ratio significantly increased in WT mice (sham: 5.78 +/- 0.55, TAC 9.79 +/- 1.82 g/mm; p
Original languageEnglish
Article numbere0150236
JournalPLOS ONE
Volume11
Issue number2
DOIs
Publication statusPublished - 26 Feb 2016

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