Angiotensin II-Treated Cardiac Myocytes Regulate M1 Macrophage Polarization via Transferring Exosomal PVT1. (1st September 2021)

• Record Type: Journal Article
• Authors: Cao, Feng; Li, Zhe; Ding, Wenmao; Yan, Ling; Zhao, Qingyan
• Other Names: Mulens Vladimir Academic Editor.
• Is Part Of: Journal of immunology research. Volume 2021(2021)
• Publication Date: 2021-09-01
• Subjects: Immunology -- Periodicals; Immunology -- Research -- Periodicals; 616.07905
• DOI: 10.1155/2021/1994328
• Languages: English
• ISSNs: 2314-8861

Abstract

Abstract : Atrial fibrillation (AF) seriously reduces the health and life quality of patients. It is necessary to explore the pathogenesis of AF and provide a new target for the treatment. Here, exosomes were identified using transmission electron microscopy and nanoparticle tracing analysis. Western blotting assay was performed to detect the expression of exosomal surface markers, extracellular matrix-related proteins, and IL-16. The expression of genes was measured using qRT-PCR. Flow cytometry was performed to examine the percentages of CD86- and CD163-positive macrophages. Besides, luciferase activity assay was performed to explore the combination between PVT1 and miR-145-5p and the combination between miR-145-5p and IL-16 3'UTR. The combination between PVT1 and miR-145-5p also was examined using RIP assay. In our study, we isolated human cardiac myocyte- (HCM-) derived exosomes successfully. Ang-II-treated HCM-derived exosomes (Ang-II-Exo) promoted M1 macrophage polarization. PVT1 was highly expressed in Ang-II-Exo. Ang-II-Exo induced macrophage to M1 polarization through transferring PVT1. Furthermore, our data showed that PVT1 increased the expression of IL-16 via sponging miR-145-5p. Finally, we proved that exosomal PVT1 could boost the extracellular matrix remodeling of atrial fibroblasts. Overall, our data demonstrated that Ang-II-Exo promoted the extracellular matrix remodeling of atrial fibroblasts via inducing M1 macrophage polarization by transferring PVT1. PVT1 facilitated M1 polarization macrophage via increasing IL-16 expression by sponging miR-145-5p. Our results provided a new evidence for PVT1 which might be a treatment target of AF.