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Experimental method for regulating and controlling EAM mouse macrophage reprogramming by Reg3beta/HMGB1 loop

A technology of N2-HMGB1, macrophages, applied in the field of immunology

Active Publication Date: 2020-07-07
NANTONG UNIVERSITY
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Problems solved by technology

Studies have shown that dedifferentiated cardiomyocytes release Reg3β when the myocardium is damaged, and then recruit monocytes / macrophages to participate in the repair of the damaged myocardium. The loss of Reg3β will delay the process of myocardial repair; Monocyte migration and infiltration when impaired are predominantly dependent on the ANG II-CCR2 / 5 axis

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  • Experimental method for regulating and controlling EAM mouse macrophage reprogramming by Reg3beta/HMGB1 loop
  • Experimental method for regulating and controlling EAM mouse macrophage reprogramming by Reg3beta/HMGB1 loop
  • Experimental method for regulating and controlling EAM mouse macrophage reprogramming by Reg3beta/HMGB1 loop

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Embodiment 1

[0098] The technical solution of the present invention will be further elaborated below with specific examples.

[0099] An experimental method for Reg3β / HMGB1 loop regulation of EAM mouse macrophage reprogramming, comprising the following steps:

[0100] Step 1. In vitro study on the effect and mechanism of Reg3β on the reprogramming and secretion of HMGB1 in myocardial infiltrating macrophages of EAM mice

[0101] 1.1. Establishment of the EAM mouse model: The EAM model was established according to the method reported in the past, that is, after fully emulsifying with MyHC-α and CFA at 1:1, BALB / c mice were immunized on the 0th day and the 7th day, respectively.

[0102] 1.2. Separation of Ly6C hi Monocytes and Ly6C hi F4 / 80+ cells: Isolate Ly6Chi mononuclear cells and Ly6C from the spleen of EAM mice hi F4 / 80+ cells (myocardial infiltrating mononuclear / Mφ mostly migrated from the spleen) and treated with 250 ng / mL Reg3β.

[0103] 1.3. The effect of Reg3β on the Mφ pheno...

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Abstract

The invention provides an experimental method for regulating and controlling EAM mouse macrophage reprogramming through a Reg3beta / HMGB1 loop. The experimental method comprises the steps of (1) researching the influence and mechanism of Reg3beta on EAM mouse myocardial infiltration macrophage reprogramming and HMGB1 secretion in vitro; (2) researching the influence and mechanism of HMGB1 on dedifferentiation, proliferation and Reg3beta release of myocardial cells in vitro; and (3) verifying the effect and mechanism of the Reg3beta / N2-HMGB1 loop in regulating and controlling macrophage reprogramming to participate in EAM mouse damaged myocardial repair in vivo. According to the invention, the interaction between myocardial cells and infiltrated M[phi] through the Reg3beta / N2-HMGB1 loop during EAM is proposed for the first time, positive feedback regulation is formed, M[phi] reprogramming is promoted to participate in damaged myocardial repair, a foundation is laid for comprehensive understanding of the effect of macrophages in the myocarditis occurrence and return process, and a new thought and a target are provided for clinical treatment of cardiovascular diseases.

Description

technical field [0001] The invention belongs to the field of immunology, and in particular relates to an experimental method for Reg3β / HMGB1 loop regulation of EAM mouse macrophage reprogramming. Background technique [0002] Myocarditis refers to localized or diffuse inflammatory lesions in the myocardium, which can be caused by various factors such as viral infection, physics, and chemistry. In recent years, the incidence of myocarditis has been increasing, and the severity of the disease varies greatly. Mild cases may have no obvious symptoms, and severe cases may be complicated by severe arrhythmia, cardiac insufficiency, cardiogenic shock or heart failure, or even sudden cardiac death, which seriously threatens human physical and mental health. Therefore, elucidating the inflammatory injury of myocarditis and the mechanism of myocardial function remodeling is of great significance for actively preventing the occurrence of myocarditis and improving people's quality of l...

Claims

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Application Information

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Patent Type & Authority Applications(China)
IPC IPC(8): G01N33/68G01N33/573
CPCG01N33/6863G01N33/6869G01N33/573Y02A50/30
Inventor 邵晓轶王守卫金晓玲
Owner NANTONG UNIVERSITY
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