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长链非编码RNA IPCRL1的敲低通过miR-185-3p/JIP3轴和JNK途径减轻心肌缺血/再灌注损伤

Knockdown of Long Noncoding RNA IPCRL1 Mitigates Myocardial Ischemia/Reperfusion Injury via miR-185-3p/JIP3 Axis and JNK Pathway.

作者信息

Chen Jingyu, Zhang Yi, Zhang Zixin, Yu Ziwei, Zhang Hao, Zhao Qifeng

机构信息

Department of Cardiovascular and Thoracic Surgery, The second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, People's Republic of China.

Wenzhou Medical University, Wenzhou, Zhejiang Province, People's Republic of China.

出版信息

J Inflamm Res. 2025 Aug 8;18:10695-10709. doi: 10.2147/JIR.S512561. eCollection 2025.

DOI:10.2147/JIR.S512561
PMID:40799798
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12341565/
Abstract

PURPOSE

Myocardial ischemia/reperfusion injury (MIRI) represents a significant culprit leading to adverse consequences after cardiac surgery. This study aims to clarify the function and related pathway of ischemic preconditioning related lncRNA-1 (IPCRL1) in MIRI.

METHODS

MIRI model was established in C57BL/6J mice via the myocardial reperfusion method, and hypoxia/reoxygenation (H/R) model was constructed using HL-1 cell. IPCRL1, miR-185-3p, JIP3, TNF-α were determined using RT-qPCR. JIP3, c-Jun, JNK phosphorylation, B-cell lymphoma 2(BCL2), Bcl-2-associated X protein (BAX), cleaved caspase-3 levels were measured using Western blot. ELISA was used to measured cardiomyocyte injury markers and TNF-α concentrations. IHC and flow cytometry investigated the trends in apoptosis. The binding relationships between IPCRL1, miR-185-3p, JIP3 were verified by Dual-luciferase reporter assay.

RESULTS

IPCRL1 knockdown reduced infarct size, inflammation, and apoptosis. Additionally, knockdown of IPCRL1 downregulates the expression of JIP3 via sponge miRNA-185-3p, thereby affecting the JNK pathway, meanwhile inhibition of miRNA-185-3p reversed above effects. Knocking down IPCRL1 can counteract cardiomyocyte apoptosis through miR-185-3p/JIP3 axis, offering protection against MIRI.

CONCLUSION

IPCRL1/miRNA-185-3p/JIP3 axis mediates MIRI through JNK pathway and IPCRL1 may hold promise as a new noteworthy target for MIRI.

摘要

目的

心肌缺血/再灌注损伤（MIRI）是心脏手术后导致不良后果的一个重要原因。本研究旨在阐明缺血预处理相关长链非编码RNA-1（IPCRL1）在MIRI中的作用及其相关通路。

方法

通过心肌再灌注法在C57BL/6J小鼠中建立MIRI模型，并用HL-1细胞构建缺氧/复氧（H/R）模型。采用RT-qPCR检测IPCRL1、miR-185-3p、JIP3、肿瘤坏死因子-α（TNF-α）。用蛋白质免疫印迹法检测JIP3、c-Jun、JNK磷酸化、B细胞淋巴瘤-2（BCL2）、Bcl-2相关X蛋白（BAX）、裂解的半胱天冬酶-3水平。用酶联免疫吸附测定法检测心肌细胞损伤标志物和TNF-α浓度。免疫组织化学和流式细胞术研究细胞凋亡趋势。通过双荧光素酶报告基因检测验证IPCRL1、miR-185-3p、JIP3之间的结合关系。

结果

敲低IPCRL1可减小梗死面积、减轻炎症和细胞凋亡。此外，敲低IPCRL1通过海绵化miRNA-185-3p下调JIP3的表达，从而影响JNK通路，同时抑制miRNA-185-3p可逆转上述作用。敲低IPCRL1可通过miR-185-3p/JIP3轴对抗心肌细胞凋亡，为MIRI提供保护。

结论

IPCRL1/miRNA-185-3p/JIP3轴通过JNK通路介导MIRI，IPCRL1有望成为MIRI一个新的重要治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de65/12341565/b66baf1ddc40/JIR-18-10695-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de65/12341565/891c46eab6dd/JIR-18-10695-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de65/12341565/801698f37e48/JIR-18-10695-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de65/12341565/afd3bd70063a/JIR-18-10695-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de65/12341565/de050f9c66a7/JIR-18-10695-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de65/12341565/139cf606284d/JIR-18-10695-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de65/12341565/00fd450047d2/JIR-18-10695-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de65/12341565/b66baf1ddc40/JIR-18-10695-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de65/12341565/891c46eab6dd/JIR-18-10695-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de65/12341565/801698f37e48/JIR-18-10695-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de65/12341565/afd3bd70063a/JIR-18-10695-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de65/12341565/de050f9c66a7/JIR-18-10695-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de65/12341565/139cf606284d/JIR-18-10695-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de65/12341565/00fd450047d2/JIR-18-10695-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de65/12341565/b66baf1ddc40/JIR-18-10695-g0007.jpg

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