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Function and application of regulatory protein G protein signal transduction 10 (rgs10) in the treatment of cardiac hypertrophy

A technology for signal transduction and protein regulation, applied in the field of gene function and application, can solve the problem of unclear role of cardiac hypertrophy diseases, and achieve the effects of inhibiting cardiac hypertrophy, anti-cardiac fibrosis cardiac hypertrophy, and protecting cardiac function.

Active Publication Date: 2018-05-15
WUHAN UNIV
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

At present, its role in cardiac hypertrophy is still unclear, and further research is needed

Method used

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  • Function and application of regulatory protein G protein signal transduction 10 (rgs10) in the treatment of cardiac hypertrophy
  • Function and application of regulatory protein G protein signal transduction 10 (rgs10) in the treatment of cardiac hypertrophy
  • Function and application of regulatory protein G protein signal transduction 10 (rgs10) in the treatment of cardiac hypertrophy

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0082] Example 1 Expression of RGS10 in the hearts of normal people and patients with cardiomyopathy

[0083] SDS-PAGE-immunoblotting test was performed on proteins extracted from the heart by selecting normal human hearts (individuals donated by non-cardiac causes of death, Donor) and hearts of patients with dilated cardiomyopathy (recipients replaced by patients undergoing heart transplantation, DCM). Western blot), combined with antibodies that specifically recognize RGS10 protein and cardiomyocyte hypertrophy markers ANP (santa cruz, #sc20158) and β-MHC (santa cruz, sc53090) to detect the expression of RGS10 (AVIVA, #ARP42856_P050) , 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 RGS10 was significantly down-regulated ( figure 1 ).

Embodiment 2

[0084] Example 2 Expression of RGS10 in the heart of wild-type mouse sham operation group and cardiac hypertrophy model group

[0085] 1. Aortic arch constriction (AB) was used to establish a mouse model of myocardial hypertrophy. The model operation process:

[0086] 1.1 Preoperative preparation

[0087] (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).

[0088] (2) Preparation of the operation area: the skin of the left chest, left chest and armpit of the left forelim...

Embodiment 3

[0099] Example 3 Expression of RGS10 in cardiomyocytes stimulated by control group (PBS) or angiotensin II (Ang II) or phenylephrine (PE)

[0100] 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 the proteins extracted from cardiomyocytes (Western blot), combined with antibodies that specifically recognize RGS10 protein and cardiomyocyte hypertrophy markers ANP and β-MHC, were used to detect the expression of RGS10, and GAPDH was used as an internal reference. Test results such as image 3 As shown, the expressions of ANP and β-MHC in card...

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Abstract

The invention discloses the function and application of G protein signal transduction regulatory protein 10 (RGS10) in the treatment of cardiac hypertrophy, belonging to the field of gene function and application. The present invention determines the relationship between the expression of RGS10 and cardiac hypertrophy, and the research results show that in the model of cardiac hypertrophy, the expression of RGS10 is significantly lower than that of the normal group; inhibiting the expression of RGS10 significantly promotes the MEK-ERK1 / 2 signaling pathway The activation of RGS10 promotes myocardial hypertrophy, fibrosis, and worsens cardiac function; overexpression of RGS10 significantly inhibits the activation of the MEK‑ERK1 / 2 signaling pathway, inhibits myocardial hypertrophy, fibrosis, and protects cardiac function. Therefore, RGS10 can be used as a target gene for screening or preparing drugs for protecting cardiac function, resisting cardiac fibrosis and / or preventing, alleviating and / or treating cardiac hypertrophy, providing an effective new way for the treatment of cardiac 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 G protein signal transduction regulatory protein 10 (RGS10) in the treatment of cardiac hypertrophy. Background technique [0002] Cardiac hypertrophy is a complex disease process regulated by multiple factors, and its mechanism has not yet been fully clarified. In the case of long-term cardiac pressure and / or volume overload, the stress of the ventricular wall increases, and the neuroendocrine system of the body also changes, and endogenous stimulation signals such as angiotensin II (Ang II), catecholamines, and endothelin are abnormal Acts on the heart, eventually leading to myocardial hypertrophy [1-3]. Clinically, many heart diseases can also cause myocardial hypertrophy [4]. Common causes include primary or secondary hypertension, valvular heart disease, coronary heart disease, and congenital heart disease. From the i...

Claims

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Application Information

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Patent Type & Authority Patents(China)
IPC IPC(8): A61K38/17A61K45/00A61P9/00G01N33/68
Inventor 李红良袁洪缪汝佳
Owner WUHAN UNIV
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