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Experimental method of long non-coding RNA up-regulation gene in myocardial hypertrophy

A technology of myocardial hypertrophy and experimental methods, applied in the field of gene coding, can solve problems such as uncertain effects of cardiac hypertrophy, and achieve the effect of reducing myocardial hypertrophy

Inactive Publication Date: 2021-05-28
张国荣
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  • Abstract
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Problems solved by technology

However, the role of the interaction between TUG1 and miR-497 in cardiac hypertrophy remains uncertain

Method used

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Embodiment Construction

[0025] The technical solutions in the embodiments of the present invention will be clearly and completely described below in conjunction with the embodiments of the present invention. Obviously, the described embodiments are only some of the embodiments of the present invention, not all of them. Based on the embodiments of the present invention, all other embodiments obtained by persons of ordinary skill in the art without making creative efforts belong to the protection scope of the present invention.

[0026] An experimental method for up-regulating genes with long non-coding RNAs in cardiac hypertrophy, comprising the following experimental steps:

[0027] Step 1: Animal care and use All animal experiment procedures were carried out in accordance with the "Guidelines for the Care and Use of Agricultural Experimental Animals". Female Sprague-Dawley (SD) rats (8 weeks old, ), kept in a pathogen-free animal breeding facility, kept all rats at a constant temperature (22±2°C), ...

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Abstract

The invention discloses an experimental method of a long non-coding RNA up-regulation gene in myocardial hypertrophy; the method is characterized in that the levels of lncRNATUG1, miR-497 and myocardial cell enhancement factor 2CmRNA are evaluated through qRT-PCR (quantitative reverse transcription-polymerase chain reaction), western blot measurement is carried out to determine the expression of MEF2C protein, and the endogenous interaction among TUG1, miR-497 and MEF2C is proved through a dual-luciferase reporter gene and RNA immunoprecipitation experiment. The overexpression of the MiR-497 mediates the protective effect of TUG1 knock-down in the cardiac hypertrophy induced by AngII. In addition, the TUG1 regulates the expression of MEF2C by spongizing miR-497. The knock-down of the TUG1 at least partially rescues AngII-induced myocardial hypertrophy by targeting the miR497 / MEF2C axis, and highlights a novel and promising therapeutic target for treating the myocardial hypertrophy.

Description

technical field [0001] The invention relates to the technical field of gene coding, in particular to an experimental method for up-regulating genes by long non-coding RNAs in cardiac hypertrophy. Background technique [0002] Cardiac hypertrophy is a common physiological compensatory response of the heart to a variety of stressors to maintain normal cardiac function. However, cardiac enlargement due to myocardial injury, hypertensive stress, or excessive neurohumoral activation is associated with maladaptive remodeling and cardiac dysfunction and is classified as pathological hypertrophy. Pathological cardiac hypertrophy is a major risk factor for dimyopathy, heart failure, and sudden cardiac death. Despite improvements in the understanding of pathological regulators in cardiac hypertrophy, the molecular mechanisms of cardiac hypertrophy remain unclear. Long noncoding RNAs (lncRNAs) are RNA molecules of more than 200 nucleotides that perform various functions in a series o...

Claims

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Application Information

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Patent Type & Authority Applications(China)
IPC IPC(8): C12N5/077C12N15/87C12N15/12C12Q1/6883A61D1/00
CPCA61D1/00C07K14/4702C12N5/0657C12N15/87C12N2509/00C12N2509/10C12Q1/6883C12Q2600/158C12Q2600/178
Inventor 张国荣倪兴华吴翔旻邓欢胡建新周裔忠
Owner 张国荣
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