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miR-29b-3p 的过表达通过靶向 PDGF-B 信号通路抑制大鼠心房重构。

Overexpression of MiR-29b-3p Inhibits Atrial Remodeling in Rats by Targeting PDGF-B Signaling Pathway.

机构信息

Department of Cardiology, Affiliated Hospital of Guilin Medical University, Guilin, 541001 Guangxi Zhuang Autonomous Region, China.

Department of Cardiology, First Affiliated Hospital of Guangxi Medical University, Nanning, 530021 Guangxi Zhuang Autonomous Region, China.

出版信息

Oxid Med Cell Longev. 2021 Jan 13;2021:3763529. doi: 10.1155/2021/3763529. eCollection 2021.

DOI:10.1155/2021/3763529
PMID:33520084
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7817267/
Abstract

PURPOSE

Studies have found that microRNAs (miRNAs) are closely associated with atrial fibrillation, but their specific mechanism remains unclear. The purpose of this experiment is to explore the function of miR-29b-3p in regulating atrial remodeling by targeting PDGF-B signaling pathway and thereby also explore the potential mechanisms.

METHODS

We randomly divided twenty-four rats into four groups. Caudal intravenous injections of angiotensin-II (Ang-II) were administered to establish atrial fibrosis models. Expressions of miR-29b-3p and PDGF-B were then tested via RT-PCR, western blot, and immunohistochemistry. Binding sites were then analyzed via the bioinformatics online software TargetScan and verified by Luciferase Reporter. We used Masson staining to detect the degree of atrial fibrosis, while immunofluorescence and western blot were used to detect the expressions of Collagen-I and a-SMA. We used immunohistochemistry and western blot to detect the expression of connexin 43 (Cx43).

RESULTS

In comparison with the Ang-II group, miR-29b-3p was seen to lower the degree of atrial fibrosis, decrease the expression of fibrosis markers such as Collagen-I and a-SMA, and increase the protein expression of Cx43. MiR-29b-3p can lower the expression of PDGF-B, while the Luciferase Reporter showed that PDGF-B is the verified target gene of miR-29b-3p.

CONCLUSIONS

MiR-29b-3p was able to reduce atrial structural and electrical remodeling in the study's rat fibrosis model. This biological function may be expressed through the targeted regulation of the PDGF-B signaling pathway.

摘要

目的

研究发现 microRNAs(miRNAs)与心房颤动密切相关,但具体机制尚不清楚。本实验旨在通过靶向 PDGF-B 信号通路探讨 miR-29b-3p 调控心房重构的功能,从而进一步探讨其潜在机制。

方法

将二十四只大鼠随机分为四组,尾静脉注射血管紧张素-II(Ang-II)建立心房纤维化模型,通过 RT-PCR、western blot 和免疫组化检测 miR-29b-3p 和 PDGF-B 的表达,通过生物信息学在线软件 TargetScan 分析结合位点,并通过 Luciferase Reporter 进行验证。采用 Masson 染色检测心房纤维化程度,免疫荧光和 western blot 检测 Collagen-I 和 a-SMA 的表达,免疫组化和 western blot 检测连接蛋白 43(Cx43)的表达。

结果

与 Ang-II 组相比,miR-29b-3p 可降低心房纤维化程度,降低 Collagen-I 和 a-SMA 等纤维化标志物的表达,增加 Cx43 蛋白表达。miR-29b-3p 可降低 PDGF-B 的表达,Luciferase Reporter 表明 PDGF-B 是 miR-29b-3p 的验证靶基因。

结论

miR-29b-3p 可减轻研究大鼠纤维化模型中的心房结构和电重构,这种生物学功能可能通过靶向调节 PDGF-B 信号通路来表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc6/7817267/7ca6e7c5847c/OMCL2021-3763529.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc6/7817267/e09e8c64f022/OMCL2021-3763529.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc6/7817267/6fb28acb8e2c/OMCL2021-3763529.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc6/7817267/7ca6e7c5847c/OMCL2021-3763529.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc6/7817267/e09e8c64f022/OMCL2021-3763529.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc6/7817267/aec7dddff768/OMCL2021-3763529.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc6/7817267/8bc39ab58c1d/OMCL2021-3763529.003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc6/7817267/6fb28acb8e2c/OMCL2021-3763529.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc6/7817267/7ca6e7c5847c/OMCL2021-3763529.007.jpg

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