Function and application of TRIM32 (Tripartite motif 32) in treating myocardial hypertrophy

A domain protein and cardiac hypertrophy technology, applied in the field of gene function and application, can solve the problems of limited clinical prevention methods and incomplete clarity of molecular regulatory network, and achieve the effect of protecting heart function

Active Publication Date: 2015-11-25
WUHAN UNIV
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

Although there is a preliminary understanding of the pathophysiological mechanism of the occurrence and development of cardiac hypertrophy, the regulatory network of its specific molecules is still not completely clear, and the clinical prevention and treatment methods are still very limited.

Method used

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  • Function and application of TRIM32 (Tripartite motif 32) in treating myocardial hypertrophy
  • Function and application of TRIM32 (Tripartite motif 32) in treating myocardial hypertrophy
  • Function and application of TRIM32 (Tripartite motif 32) in treating myocardial hypertrophy

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0081] EXAMPLE 1 Expression of TRIM32 in the hearts of normal people and patients with dilated heart

[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 specifically recognizing TRIM32 protein and cardiomyocyte hypertrophy markers ANP (Millipore, AB2232) and Myh7 (santacruz, sc53090) were detected to measure the expression of TRIM32 (ProSci, 28-984), and GAPDH (Cell Signaling Technology, 2128) was used as an internal reference . Test results such as figure 1 As shown, the expression of cardiomyocyte hypertrophy markers ANP and Myh7 in the hearts of patients with dilated cardiomyopathy was significantly up-regulated, and the expression of TRIM32 was significantly down-regulated.

Embodiment 2

[0083] Example 2 Expression of TRIM32 in wild-type mouse sham operation group and cardiac hypertrophy model group hearts

[0084] 1. The mouse myocardial hypertrophy model is modeled by aortic arch constriction (AB), and the model operation process is as follows:

[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 for...

Embodiment 3

[0098] Example 3 Expression of TRIM32 in cardiomyocytes stimulated by control group (PBS) or angiotensin II (AngII) 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 After starving cardiomyocytes for 12 hours to synchronize the cells, they were stimulated with PBS, angiotensin II (AngII, 1 μM) and phenylephrine (PE, 1 μM) for 48 hours, and SDS-PAGE-immunoblotting was performed on proteins extracted from cardiomyocytes ( Western blot), combined with antibodies that specifically recognize TRIM32 protein and cardiomyocyte hypertrophy markers ANP and Myh7, were used to detect the expression of TRIM32, and GAPDH was used as an internal reference. Test results such as image 3 As shown, the expressions of ANP and Myh7 in cardiom...

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Abstract

The invention discloses a function and an application of TRIM32 (Tripartite motif 32) in treating myocardial hypertrophy and belongs to the field of gene functions and applications. The mutual relation between expression of TRIM32 and myocardial hypertrophy is determined, a research result proves that in a model where myocardial hypertrophy occurs, the expression of TRIM 32 is remarkably reduced than that of a normal group; if expression of TRIM 32 is inhibited, activation of an AKT signal path is remarkably promoted, myocardial hypertrophy and fibrosis are promoted, and the cardiac function is deteriorated; if overexpression of TRIM 32 is promoted, activation of the AKT signal path is remarkably inhibited, myocardial hypertrophy and fibrosis are inhibited, and the cardiac function is protected. Therefore, TRIM32 can be taken as a target gene and used for screening or preparing a drug for protecting the cardiac function, preventing cardiac fibrosis and / or preventing, relieving and / or treating myocardial hypertrophy, and a new effective way is provided for treatment of myocardial hypertrophy.

Description

technical field [0001] The invention belongs to the field of gene function and application, and particularly relates to the function and application of a triple domain protein 32 (TRIM32) in the treatment of cardiac hypertrophy. Background technique [0002] Myocardial hypertrophy is the increase in the size and weight of cardiomyocytes produced by the heart in response to various long-term excessive pressure and / or volume load stimuli. In myocardial hypertrophy, due to increased protein synthesis, cardiomyocytes increase in size, diameter or length, and the number of sarcomeres increases. At the same time, the phenotype of cardiomyocytes also changes from mature to embryonic, accompanied by proliferation of myocardial mesenchymal cells and remodeling of cardiac extracellular matrix, resulting in myocardial remodeling[1,2]. Clinically, many heart diseases can cause myocardial hypertrophy. Common causes include primary or secondary hypertension, valvular heart disease, coron...

Claims

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Application Information

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Patent Type & Authority Applications(China)
IPC IPC(8): A61K38/17A61K45/00C12Q1/68A61P9/04A61P9/00
Inventor 李红良陈立娟黄嘉张晓晶
Owner WUHAN UNIV
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