LncRNA AK045171 protects the heart from cardiac hypertrophy by regulating the SP1/MG53 signalling pathway.

Abstract

Hearts often undergo abnormal remodelling and hypertrophic growth in response to pathological stress. Long non-coding RNAs (LncRNAs) can change cardiac function and participate in regulation of cardiac hypertrophy. The present study aims to identify the role of AK045171 in cardiac hypertrophy and the underlying mechanism in hypertrophic cascades. Mice with cardiac hypertrophy were established through transverse aortic constriction (TAC). Cardiac hypertrophy in cardiomyocytes was induced by angiotensin II (angII). The expression of AK045171 and its target gene SP1 was examined in cardiomyocytes transfected with miRNA. The AK045171 expression level was downregulated in mice after TAC surgery. Overexpression of AK045171 attenuated cardiac hypertrophy both in vitro and in vivo. The mechanism study indicated that AK045171 binds with SP1, which promotes transcription activation of MEG3. It is suggested that overexpression of AK045171 might have clinical potential to suppress cardiac hypertrophy and heart failure.

• Authors: Li Xu, Hongjiang Wang, Feng Jiang, Hao Sun, Dapeng Zhang
• Journal: Aging (Aging (Albany NY)) Vol. 12 Issue 4 Pg. 3126-3139 (02 21 2020) ISSN: 1945-4589 [Electronic] United States
• PMID: 32087602 (Publication Type: Journal Article, Retracted Publication)

Chemical References

• MG53 protein, mouse
• Membrane Proteins
• RNA, Long Noncoding
• Sp1 Transcription Factor
• Angiotensin II

Topics

• Angiotensin II (pharmacology)
• Animals
• Cardiomegaly (metabolism)
• Disease Models, Animal
• Down-Regulation
• Membrane Proteins (metabolism)
• Mice
• Myocardium (metabolism)
• Myocytes, Cardiac (drug effects, metabolism)
• RNA, Long Noncoding (metabolism)
• Signal Transduction (physiology)
• Sp1 Transcription Factor (metabolism)