Function and application of mitochondria-associated ribosomal GTPase 1 (MTG1) in the treatment of cardiac hypertrophy

A myocardial hypertrophy and ribosome technology, applied in the field of gene function and application, can solve the problems of lack of research, decreased expression of respiratory chain complex I and IV, decreased mitochondrial DNA translation level, etc., to protect heart function and inhibit myocardial hypertrophy , the effect of anti-cardiac fibrosis and myocardial hypertrophy

Active Publication Date: 2018-09-21
WUHAN UNIV
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

In 2013, Tetsuya Kotani et al. further proved at the cellular level that the decrease in the expression of MTG1 would lead to a decrease in the translation of mitochondrial DNA, resulting in a decrease in the expression of respiratory chain complexes I and IV.
However, the role of MTG1 in heart disease is still not studied [22]

Method used

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  • Function and application of mitochondria-associated ribosomal GTPase 1 (MTG1) in the treatment of cardiac hypertrophy
  • Function and application of mitochondria-associated ribosomal GTPase 1 (MTG1) in the treatment of cardiac hypertrophy
  • Function and application of mitochondria-associated ribosomal GTPase 1 (MTG1) in the treatment of cardiac hypertrophy

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0081] Example 1 Expression of MTG1 in the hearts of normal people and patients with cardiomyopathy

[0082] Select normal human hearts (individuals donated by non-cardiac causes of death) and dilated cardiomyopathy patients’ hearts (recipients replaced by patients undergoing heart transplantation), and perform SDS-PAGE-Western blot test (Western blot) on proteins extracted from the hearts, combined with Antibodies that specifically recognize MTG1 protein and cardiomyocyte hypertrophy markers ANP (Millipore, AB2232) and β-MHC (santa cruz, sc53090) were detected to measure the expression of MTG1 (santa cruz, sc160545), and GAPDH (Cell Signaling Technology, 2128) as an internal reference. Test results such as figure 1 As shown, the expression of cardiomyocyte hypertrophy markers ANP and β-MHC in the hearts of patients with dilated cardiomyopathy was significantly up-regulated, and the expression of MTG1 was significantly up-regulated ( figure 1 ).

Embodiment 2

[0083] Example 2 Expression of MTG1 in the heart of wild-type mouse sham operation group and cardiac hypertrophy model group

[0084] 1. Aortic arch constriction (AB) was used to establish a mouse model of myocardial hypertrophy. The model operation process:

[0085] 1.1 Preoperative preparation

[0086] (1) Anesthesia: First weigh the mice, calculate the required amount of anesthetic (3% pentobarbital sodium) according to 90 mg / kg body weight, inject intraperitoneally, and record the injection time point. There is no obvious reaction between tail and toe pinching and the mouse is in good condition. This is the standard for successful anesthesia (generally there is no obvious reaction about 10 minutes after injection, and the mouse has a reaction to pinch toe about 50 minutes after anesthesia, and about 30 minutes after anesthesia is the best operation time).

[0087] (2) Preparation of the operation area: the skin of the left chest, left chest and armpit of the left forelimb...

Embodiment 3

[0098] Example 3 Expression of MTG1 in cardiomyocytes stimulated by control group (PBS) or angiotensin II (Ang II) or phenylephrine (PE)

[0099] Isolate and culture newborn 1-day Sprague-Dawley neonatal rat cardiomyocytes, culture the primary cardiomyocytes for 48 hours and change the medium (see the following example 4 for the specific process of primary neonatal SD rat cardiomyocyte culture), add serum-free DMEM / F12 Starve the cardiomyocytes for 12 hours to synchronize the cells, give PBS, angiotensin II (Ang II, 1 μM) and phenylephrine (PE, 1 μM) stimulation for 48 hours respectively, and perform SDS-PAGE-immunoblotting test on proteins extracted from cardiomyocytes (Western blot), combined with antibodies that specifically recognize MTG1 protein and cardiomyocyte hypertrophy markers ANP and β-MHC to detect the expression of MTG1, GAPDH was used as an internal reference, and the detection results were as follows image 3 As shown, the expressions of ANP and β-MHC in cardio...

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Abstract

The invention discloses functions and application of ribosome GTP enzyme 1 (MTG1) relevant to mitochondria to treatment of myocardial hypertrophy and belongs to the field of functions and application of genes. The mutual relation between expression of MTG1 and myocardial hypertrophy is determined, and the research result shows that in a model where myocardial hypertrophy happens, expression of MTG1 is remarkably reduced compared with a normal group; when expression of MTG1 is inhibited, myocardial hypertrophy and fibrosis are remarkably promoted, and the heart function is deteriorated; when over-expression of MTG1 is promoted, myocardial hypertrophy and fibrosis are remarkably inhibited, and the heart function is protected. Thus, MTG1 can serve as target genes, are used for screening drugs for protecting the heart function, resisting cardiac fibrosis and / or preventing and relieving and / or treating myocardial hypertrophy and are used for preparing drugs for protecting the heart function, resisting cardiac fibrosis and / or preventing and relieving and / or treating myocardial hypertrophy, and a new effective path is provided for treating myocardial hypertrophy.

Description

technical field [0001] The invention belongs to the field of gene function and application, and in particular relates to the function and application of a mitochondrial-associated ribosomal GTPase 1 (MTG1) in the treatment of cardiac hypertrophy. Background technique [0002] Myocardial hypertrophy is the compensatory response of the myocardium to long-term biomechanical pressure or increased volume load, which is commonly seen in cardiovascular diseases such as hypertension and aortic stenosis. Increased and other characteristics [1-3]. Hypertension and senile degenerative aortic valve disease are on the rise year by year in our country. Cardiac hypertrophy and the incidence of hypertension and heart disease caused by hypertension and other diseases also increase thereupon. Although myocardial hypertrophy can initially increase myocardial cells and strengthen myocardial contractility, which is a compensatory mechanism to maintain normal cardiac output, long-term continuou...

Claims

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Application Information

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Patent Type & Authority Patents(China)
IPC IPC(8): A61K48/00A61K38/43A61P9/00G01N33/68
Inventor 李红良徐亚伟赵逸凡王丕晓张晓晶
Owner WUHAN UNIV
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