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Function and application of three-domain protein 8 (trim8) inhibitor in inhibiting cardiac hypertrophy

A myocardial hypertrophy and inhibitor technology, applied in the field of gene function and application, can solve the problem of no TRIM8 research report and other problems, and achieve the effect of promoting myocardial hypertrophy

Active Publication Date: 2017-03-08
WUHAN UNIV
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

Studies have found that TRIM8 can participate in various pathophysiological processes including innate immune response and tumorigenesis by regulating key signaling pathway molecules such as SOCS1, TAK1, PIAS3 and P53[11-15], but there is still no TRIM8 in the cardiovascular system. Related research reports on the role in disease

Method used

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  • Function and application of three-domain protein 8 (trim8) inhibitor in inhibiting cardiac hypertrophy
  • Function and application of three-domain protein 8 (trim8) inhibitor in inhibiting cardiac hypertrophy
  • Function and application of three-domain protein 8 (trim8) inhibitor in inhibiting cardiac hypertrophy

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0077] Example 1 Expression of TRIM8 in the hearts of normal people and patients with dilated heart

[0078] Select normal human hearts (individuals donated by non-cardiac causes of death) and dilated cardiomyopathy patients’ hearts (recipients replaced by patients undergoing heart transplantation). Antibodies that specifically recognize TRIM8 protein and cardiomyocyte hypertrophy markers ANP (Millipore, AB2232) and Myh7 (santa cruz, sc53090) were detected to measure the expression of TRIM8 (ProSci, 25-217), and GAPDH (Cell Signaling Technology, 2128 ) as an internal reference. Test results such as figure 1 As shown, the expressions of cardiomyocyte hypertrophy markers ANP and Myh7 were significantly up-regulated in the hearts of patients with dilated cardiomyopathy, and the expression of TRIM8 was also significantly up-regulated ( figure 1 ).

Embodiment 2

[0079] Example 2 Expression of TRIM8 in the heart of wild-type mouse sham operation group and cardiac hypertrophy model group

[0080] 1. The mouse model of cardiac hypertrophy is modeled by aortic arch constriction (AB). The operation procedure of the model is as follows:

[0081] 1.1 Preoperative preparation

[0082] (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).

[0083] (2) Preparation of the operation area: the skin of the left chest, left chest and armpit of th...

Embodiment 3

[0094] Example 3 Expression of TRIM8 in cardiomyocytes stimulated by control group (PBS) or angiotensin II (Ang II) or phenylephrine (PE)

[0095] 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 cardiomyocytes for 12 hours to synchronize the cells, give PBS, angiotensin angiotensin II (Ang II, 1 μM) and phenylephrine (PE, 1 μM) respectively to stimulate for 48 hours, and perform SDS-PAGE- Western blot was used to detect the expression of TRIM8 by combining antibodies that specifically recognize TRIM8 protein and cardiomyocyte hypertrophy markers ANP and Myh7, and GAPDH was used as an internal reference. Test results such as image 3 As shown, the expressions of ANP and Myh7 were significantly up-regulated in cardiomyocytes stimulated by angiote...

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Abstract

The invention discloses a function and an application of a TRIM8 (tripartite motif 8) inhibitor in inhibition of myocardial hypertrophy and belongs to the field of genetic functions and applications. The correlation between TRIM8 expression and myocardial hypertrophy is determined, research results show that TRIM8 expression is increased remarkably compared with a normal group in a model with myocardial hypertrophy; myocardial hypertrophy and fibrosis are inhibited remarkably and cardiac functions are protected through inhibition of TRIM8 expression, and myocardial hypertrophy and fibrosis are promoted remarkably and the cardiac functions are deteriorated through promotion of TRIM8 overexpression. Therefore, the TRIM8 can be taken as a drug target to be used for screening drugs for protecting the cardiac functions, resisting cardiac fibrosis and / or preventing, relieving and / or treating myocardial hypertrophy; the TRIM8 inhibitor is used for preparing drugs for protecting the cardiac functions, resisting myocardial hypertrophy and / or preventing, relieving and / or treating myocardial hypertrophy, and a new effective way for treatment of myocardial hypertrophy is provided.

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 8 (TRIM8) inhibitor in inhibiting 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, co...

Claims

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Application Information

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Patent Type & Authority Patents(China)
IPC IPC(8): G01N33/68A61K45/00A61P9/00A61P9/04
CPCA61K45/00G01N33/6893G01N2333/47G01N2800/32
Inventor 李红良陈立娟黄嘉张晓晶
Owner WUHAN UNIV
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