In both models, Miat-KO mice displayed reduced heart-weight to tibia-length ratio, cardiomyocyte cross-sectional area, cardiomyocyte apoptosis, and cardiac interstitial fibrosis and a better-preserved capillary density, as compared to WT mice. Surgical TAC for 6 weeks resulted in decreased systolic function and heart failure in WT mice but not in Miat-KO mice. Results: Continuous Ang II infusion for 4 weeks induced concentric hypertrophy in WT mice, but to a lesser extent in Miat-KO mice. Primary WT and Miat-KO mouse cardiomyocytes were isolated and used in Ca 2+ transient and contractility measurements. Gene expression in the heart was evaluated by RNA sequencing (RNA-seq), quantitative real-time RT-PCR (qRT-PCR), and Western blotting. Heart structure and function were evaluated by echocardiography and histological assessments. Methods: Both an angiotensin II (Ang II) infusion model and a transverse aortic constriction (TAC) model were used in adult WT and Miat-null knockout ( Miat-KO) mice to induce pathological cardiac hypertrophy. Here we investigated whether Miat regulates cardiac response to pathological hypertrophic stimuli. Rationale: The conserved long non-coding RNA (lncRNA) myocardial infarction associate transcript ( Miat) was identified for its multiple single-nucleotide polymorphisms that are strongly associated with susceptibility to MI, but its role in cardiovascular biology remains elusive. Select the file that you have just downloaded and select import option Reference Manager (RIS). Ablation of lncRNA Miat attenuates pathological hypertrophy and heart failure. Yang L, Deng J, Ma W, Qiao A, Xu S, Yu Y, Boriboun C, Kang X, Han D, Ernst P, Zhou L, Shi J, Zhang E, Li TS, Qiu H, Nakagawa S, Blackshaw S, Zhang J, Qin G. ✉ Corresponding author: Gangjian Qin, MD, FAHA, Department of Biomedical Engineering, School of Medicine & School of Engineering, University of Alabama at Birmingham, 1720 2nd Ave S, Volker Hall G094N, Birmingham, AL 35294, USA. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo 060-0812, Japan.Ĩ. Center for Molecular and Translational Medicine, Institute of Biomedical Science, Georgia State University, Atlanta, GA 30303, USA.ħ. Department of Stem Cell Biology, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki 852-8523, Japan.Ħ. Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USAĥ. Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.Ĥ. Feinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.ģ. Molecular Cardiology Program, Department of Biomedical Engineering, University of Alabama at Birmingham, School of Medicine and School of Engineering, Birmingham, AL 35294, USA.Ģ. Liu Yang 1,2,3, Jianxin Deng 1, Wenxia Ma 1, Aijun Qiao 1, Shiyue Xu 1, Yang Yu 2, Chan Boriboun 1, Xiang Kang 1, Dunzheng Han 1, Patrick Ernst 1, Lufang Zhou 1,4, Jiawei Shi 1, Eric Zhang 1, Tao-Sheng Li 5, Hongyu Qiu 6, Shinichi Nakagawa 7, Seth Blackshaw 8, Jianyi Zhang 1, Gangjian Qin 1,2ġ. Research Paper Ablation of lncRNA Miat attenuates pathological hypertrophy and heart failure

Pathological hypertrophy heart diagram