Application of Ckip-1 3' UTR in medicine for preventing and/or treating heart failure disease

A 1.ckip-13, heart failure technology, applied in the fields of molecular biology and medicine, can solve problems such as the role of which is poorly understood, and achieve the effect of preventing heart failure and alleviating changes in remodeling indicators

Active Publication Date: 2021-10-29
SCI RES TRAINING CENT FOR CHINESE ASTRONAUTS
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

Although lncRNAs have been reported to be involved in the pathogenesis of various cardiac diseases, the role of non-coding RNA 3′UTR in the mRNA component remains poorly understood

Method used

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  • Application of Ckip-1 3' UTR in medicine for preventing and/or treating heart failure disease
  • Application of Ckip-1 3' UTR in medicine for preventing and/or treating heart failure disease
  • Application of Ckip-1 3' UTR in medicine for preventing and/or treating heart failure disease

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0073] Ckip-1 3′UTR overexpression affects the cardiac phenotype of swimming-induced physiological cardiac hypertrophy in mice:

[0074] (1) Swimming exercise model in mice: Swimming exercise is used to simulate physiological cardiac hypertrophy in mice. Pour clean water into the pool and heat it to make the water temperature reach 25±1°C. Nine days before the experiment was the adaptation period for the mice to swim. From the first day, they trained once in the morning and in the afternoon, each time for 10 minutes. After the test, the mice were wiped dry. In the future, I always insist on one time in the morning and one in the afternoon every day, but add 10 minutes to each swimming training, until the ninth day, I swim for 90 minutes each time. Afterwards, the mice in each group entered the formal swimming exercise for 12 days, once in the morning and in the afternoon for 90 minutes each, and the swimming exercise experiment lasted for 21 days. It should be noted that the...

Embodiment 2

[0078] Ckip-1 3′UTR overexpression affects the cardiac phenotype of TAC-induced pathological cardiac hypertrophy in mice

[0079] (1) Extract the RNA in each tissue of WT mice and 3′UTR TG mice, and perform real-time fluorescent quantitative PCR to detect the expression of Ckip-1 3′UTR in various tissues of mice after reverse transcription. The primer sequences of 'UTR are shown in Table 5.

[0080] table 5

[0081] Mouse Gapdh-F SEQ NO.2: 5'-actccactcacggcaaattca-3' Mouse Gapdh-R SEQ NO.3: 5'-ggcctcaccccatttgatg-3' Mouse Ckip-1 3′UTR-F SEQ NO.4: 5'-gggggcaggtctgaaat-3' Mouse Ckip-1 3′UTR-R SEQ NO.5: 5'-tgcaacatttggagataaagag-3'

[0082] The expression results of Ckip-1 3′UTR in various tissues of mice are as follows: Figure 4 As shown, the results showed that Ckip-1 3′UTR was specifically highly expressed in the heart tissue of 3′UTR TG mice.

[0083] (2) WT mice and 3′UTR TG mice were subjected to cardiac histopathological analysis, a...

Embodiment 3

[0090] Effect of intravenous administration of Ckip-1 3′UTR packaged with adeno-associated virus on myocardial hypertrophy induced by TAC

[0091] (1) Construction of Ckip-1 3′UTR packaged by adeno-associated virus: Burn Ckip-1 3′UTR into the adeno-associated virus vector AAV9 with a cardiac-specific promoter to construct Ckip-1 3′UTR packaged by adeno-associated virus UTR (AAV9-cTNT-3'UTR). Virus construction, packaging and purification were completed by Hanbio.

[0092] (2) TAC operation was performed on WT mice, and AAV9-cTNT-3′UTR (1*10 11 vg / only), echocardiography was performed three weeks later. The results of left ventricular ejection fraction EF and short-axis shortening rate FS after 4 weeks of TAC are as follows: Figure 12 and 13As shown, the results showed that the injection of AAV9-cTNT-3'UTR could counteract the decline in cardiac function caused by TAC.

[0093] (3) Histopathological analysis of the heart of WT mice after 4 weeks of TAC, the results of Mas...

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Abstract

The invention relates to application of Ckip-1 3' UTR in a medicine for preventing and/or treating a heart failure disease, and belongs to the technical field of molecular biology and medicine. The research finds that Ckip-1 3' UTR overexpression promotes beneficial physiological myocardial hypertrophy. The application of Ckip-1 3' UTR in screening or preparing a medicine target for the beneficial physiological myocardial hypertrophy is achieved. Meanwhile, the Ckip-1 3' UTR overexpression has a protection effect on pathological myocardial hypertrophy and heart failure caused by TAC. The application of Ckip-1 3' UTR in screening or preparing the medicine target for preventing and/or treating the heart failure disease is achieved. The application of Ckip-1 3' UTR as a treatment target for preventing and/or treating the heart failure disease or as a diagnosis target for the heart failure disease is achieved.

Description

technical field [0001] The invention relates to the application of Ckip-1 3'UTR in medicines for preventing and / or treating heart failure diseases, and belongs to the technical field of molecular biology and medicine. Background technique [0002] Heart failure is a growing public health problem and a leading cause of morbidity and mortality in modern society. Cardiac hypertrophy is an important precursor to heart failure, which will eventually lead to heart failure. Cardiac hypertrophy is characterized by enlarged cardiomyocytes, increased protein synthesis, reactivation of fetal genes, cytoskeletal remodeling, and enhanced fibrosis. Clinically, it is manifested as impaired myocardial systolic and diastolic function, reduced ejection fraction and other cardiac insufficiency. However, current treatment and prognosis of heart failure remain seriously ill. Therefore, with the increasing burden of heart failure, it is urgent to further deepen the research on the disease proc...

Claims

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Application Information

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Patent Type & Authority Applications(China)
IPC IPC(8): A61K45/00A61P9/04C12Q1/6883
CPCA61K45/00A61P9/04C12Q1/6883C12Q2600/136C12Q2600/158Y02A50/30
Inventor 李英贤凌树宽赵银龙
Owner SCI RES TRAINING CENT FOR CHINESE ASTRONAUTS
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