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Downregulation of MicroRNA-29-3p Following Percutaneous Coronary Intervention: An Implication of YY1/IRAK1 Pathway in
Yunying Zhou1, Yong Yang2, Lang Hong1
1Department of Cardiology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi.
Abstract:
This study explored the expression of microRNA (miR)-29b-3p following percutaneous coronary intervention (PCI) and the implication of its downstream Yin Yang 1 (YY1)/interleukin (IL)-1 receptor-associated kinase 1 (IRAK1) pathway in post-vascular injury inflammation. Blood samples were collected for analysis of plasma miR-29b-3p from patients with acute coronary syndrome before surgery, 1 day after PCI, and 30 days after PCI. Lipopolysaccharide (LPS)-treated human coronary artery endothelial cells (HCAECs) were transfected with miR-29b-3p mimic/inhibitor or YY1 shRNA and underwent viability tests. Enzyme-linked immunosorbent assay was performed to detect the levels of soluble vascular cell adhesion molecule-1 (sVCAM-1), IL-1β, IL-6, and tumor necrosis factor (TNF)-α in serum and cell culture supernatant. Dual-luciferase reporter and RNA/chromatin immunoprecipitation were used to confirm the targeting relationships among miR-29b-3p, YY1, and IRAK1. A rat model of intraluminal injury of the common femoral artery was established to address the role of miR-29b-3p and relevant mechanisms. miR-29b-3p was lowly expressed, and sVCAM-1, IL-1β, IL-6, and TNF-α were upregulated 1 day after PCI and 24 h after LPS treatment. miR-29b-3p overexpression or YY1 knockdown alleviated LPS-induced inflammatory responses and improved the viability of HCAECs. miR-29b-3p inhibition aggravated LPS-induced inflammatory injury in HCAECs. miR-29b-3p bound to YY1 mRNA and inhibited the expression of YY1 protein. YY1 bound to the IRAK1 promoter and activated the transcription of IRAK1. Upregulation of miR-29b-3p suppressed the inflammatory response after intraluminal injury of the common femoral artery in rats. In conclusion, dysregulation of the YY1/IRAK1 pathway via miR-29b-3p downregulation may be implicated in post-vascular injury inflammation.
Insights
MicroRNA (miR)-29b-3p downregulation exacerbates vascular injury inflammation by activating the Yin Yang 1 (YY1)/interleukin-1 receptor-associated kinase 1 (IRAK1) pathway. Restoring miR-29b-3p levels suppresses inflammation.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Inflammation Research
Background:
- Percutaneous coronary intervention (PCI) can trigger post-vascular injury inflammation.
- MicroRNAs (miRNAs) play crucial roles in regulating cellular processes, including inflammation.
- The specific role of miR-29b-3p in vascular inflammation post-PCI requires elucidation.
Purpose of the Study:
- To investigate the expression of miR-29b-3p after PCI.
- To explore the involvement of the miR-29b-3p/Yin Yang 1 (YY1)/interleukin-1 receptor-associated kinase 1 (IRAK1) pathway in post-vascular injury inflammation.
- To determine the therapeutic potential of modulating miR-29b-3p in vascular inflammation.
Main Methods:
- Analysis of plasma miR-29b-3p levels in patients undergoing PCI.
- In vitro studies using lipopolysaccharide (LPS)-treated human coronary artery endothelial cells (HCAECs) with miR-29b-3p mimic/inhibitor or YY1 shRNA.
- In vivo studies using a rat model of common femoral artery injury.
- Detection of inflammatory markers (sVCAM-1, IL-1β, IL-6, TNF-α) using ELISA.
- Confirmation of molecular interactions using dual-luciferase reporter and RNA/chromatin immunoprecipitation assays.
Main Results:
- miR-29b-3p expression was downregulated post-PCI and after LPS treatment.
- Overexpression of miR-29b-3p or knockdown of YY1 reduced LPS-induced inflammation and improved HCAEC viability.
- Inhibition of miR-29b-3p aggravated inflammatory responses.
- miR-29b-3p directly targets YY1, and YY1 activates IRAK1 transcription.
- Upregulation of miR-29b-3p attenuated inflammation in a rat vascular injury model.
Conclusions:
- Downregulation of miR-29b-3p contributes to post-vascular injury inflammation by activating the YY1/IRAK1 pathway.
- miR-29b-3p acts as a negative regulator of vascular inflammation.
- Modulating miR-29b-3p may offer a therapeutic strategy for managing post-PCI inflammation.
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