TY - JOUR
T1 - Long Non-Coding RNA Malat-1 Is Dispensable during Pressure Overload-Induced Cardiac Remodeling and Failure in Mice
AU - Peters, Tim
AU - Beijnsberger, Steffie
AU - Beqqali, Abdelaziz
AU - Bitsch, Nicole
AU - Nakagawa, Shinichi
AU - Prasanth, Kannanganattu V.
AU - de Windt, Leon J.
AU - van Oort, Ralph J.
AU - Heymans, Stephane
AU - Schroen, Blanche
PY - 2016/2/26
Y1 - 2016/2/26
N2 - 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
AB - 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
U2 - 10.1371/journal.pone.0150236
DO - 10.1371/journal.pone.0150236
M3 - Article
C2 - 26919721
VL - 11
JO - PLOS ONE
JF - PLOS ONE
SN - 1932-6203
IS - 2
M1 - e0150236
ER -