Discovered in the late 1980s as an extracellular vesicle of endosomal origin secreted from reticulocytes, exosomes recently gained scientific attention due to its role in intercellular communication. Exosomes have now been identified to carry cell-specific cargo of nucleic acids, proteins, lipids, and other biologically active molecules. Exosomes can be selectively taken up by neighboring or distant cells, which has shown to result in structural and functional responses in the recipient cells. Recent advances indicate the regulation of exosomes at various steps, including their biogenesis, selection of their cargo, as well as cell-specific uptake. This review will shed light on the differences between the type of extracellular vesicles. In this review, we discuss the recent progress in our understanding of the regulation of exosome biogenesis, secretion, and uptake.

https://link.springer.com/content/pdf/10.1007/s11010-020-03703-z.pdf

Inside(sight) of tiny communicator: exosome biogenesis, secretion, and uptake

Exosomes are nanosized lipid vesicles originating from the endosomal system that carry many macromolecules from their parental cells and play important roles in intercellular communication. The functions and underlying mechanisms of exosomes in atherosclerosis have recently been intensively studied. In this review, we briefly introduce exosome biology and then focus on advances in the roles of exosomes in atherosclerosis, specifically exosomal changes associated with atherosclerosis, their cellular origins and potential functional cargos, and their detailed impacts on recipient cells. We also discuss the potential of exosomes as biomarkers and drug carriers for managing atherosclerosis.

Exosomes in atherosclerosis: performers, bystanders, biomarkers, and therapeutic targets.

Cardiac exosomes mediate cell-to-cell communication, stimulate or inhibit the activities of target cells, and affect myocardial hypertrophy, injury and infarction, ventricular remodeling, angiogenesis, and atherosclerosis. The exosomes that are released in the heart from cardiomyocytes, vascular cells, fibroblasts, and resident stem cells are hypoimmunogenic, are physiologically more stable than cardiac cells, can circulate in the body, and are able to cross the blood-brain barrier. Exosomes utilize three mechanisms for cellular communication: (1) internalization by cells, (2) direct fusion to the cell membrane, and (3) receptor-ligand interactions. Cardiac exosomes transmit proteins, mRNA, and microRNAs to other cells during both physiological and pathological process. Cardiac-specific exosome miRNAs can regulate the expression of sarcomeric genes, ion channel genes, autophagy, anti-apoptotic and anti-fibrotic activity, and angiogenesis. This review discusses the role of exosomes and microRNAs in normal myocardium, myocardial injury and infarction, atherosclerosis, and the importance of circulating microRNAs as biomarkers of cardiac disease. Graphical Abstract.

Cardiovascular Exosomes and MicroRNAs in Cardiovascular Physiology and Pathophysiology

Background Tumor microenvironment (e.g., cancer-associated fibroblast) plays a key role in cancer tumorigenesis and metastasis. However, the detailed mechanism of whether hypoxia promotes CRC progression via tumor microenvironment remains unclear. Methods In this study, circEIF3K exosome was examined by NanoSight Tracking Analysis and RT-qPCR. We used cell colony formation assay, transwell assay and tube formation assay to determine proliferation, invasion and metastasis of HCT116 or SW620 cells. Xenograft tumor assay was employed to show in vivo tumor growth of HCT116 cells. Results We found that hypoxia could induce secretion of circEIF3K exosome. Conditioned medium (CM) and exosome from circEIF3K knockdown CAF significantly attenuated proliferation, invasion and tube formation of HCT116 or SW620 cells, which could be reverted by miR-214 under hypoxia treatment. Besides, we observed that circEIF3K knockdown evidently impaired tumor growth in mice. TCGA dataset analysis showed that low expression of circEIF3K was observed in normal tissues and associated with prolonged survival time. Finally, PD-L1 was confirmed as important target for miR-214 in CRC. Conclusion In conclusion, our study reveals that a novel axis circEIF3K/miR-214/PD-L1 mediates hypoxia-induced CRC progression via CAF, providing the rationale for developing new targeted therapeutics to treat CRC.

/pdf/exosomal-circeif3k-from-cancer-associated-fibroblast-430crbulve.pdf

Exosomal circEIF3K from cancer-associated fibroblast promotes colorectal cancer (CRC) progression via miR-214/PD-L1 axis.

Atherosclerosis (AS) is a chronic inflammatory disease of the vascular wall with multiple causes. AS is the primary pathological basis of cardiovascular disease and stroke. Moreover, carotid plaque rupture and thrombus formation are the main causes of ischemic stroke. Therefore, understanding the formation of carotid plaques may help improve the prediction and prevention of cardiovascular and cerebrovascular events. Endothelial cell dysfunction results in re‑endothelialization and angiogenesis in atherosclerotic plaques, thus promoting plaque destabilization. The aim of the present study was to evaluate the effect of circular RNA (circRNA) molecules in serum exosomes (serum‑Exos) from patients with stable plaque atherosclerosis (SA) and unstable/vulnerable plaque atherosclerosis (UA). Specifically, the effect of circRNA on human umbilical vein endothelial cell (HUVEC) behavior and the mechanisms underlying plaque destabilization in AS were evaluated. Serum‑Exos were isolated, then identified using transmission electron microscopy, nanoparticle tracking analysis and western blotting. The serum‑Exo‑circRNA expression profile of patients with SA or UA was investigated using a circRNA array. The relationship between circRNA‑006896 in serum‑Exos and biochemical parameters of patients with SA and UA were analyzed using Spearman's correlation. In addition, HUVECs were incubated with serum‑Exos for in vitro functional assays. The present study demonstrated that circRNAs expression profiles in SA and UA serum‑Exos were significantly different, indicating a potential role for circRNAs in carotid plaque destabilization. The expression of circRNA‑0006896 was positively correlated with triglyceride, low‑density lipoprotein cholesterol (LDL‑C) and C‑reactive protein levels, and negatively correlated with albumin levels in patients with UA. However, circRNA‑0006896 expression was positively correlated with LDL‑C in patients with SA. Using bioinformatic analysis, a competing endogenous RNA (ceRNA) network was selected to study the regulatory roles of circRNA‑0006896 in serum‑Exos. Additionally, in HUVECs treated with serum‑Exos derived from patients with UA, the expression of circRNA‑0006896 in HUVECs was upregulated. This was accompanied by decreased expression of microRNA‑1264 and SOCS3, increased levels of DNMT1 and phosphorylated STAT3. HUVEC proliferation and migration were significantly increased in the UA group, compared with the mock and SA groups. This finding indicates that the circRNA‑0006896‑miR-1264‑DNMT1 axis plays an important role in carotid plaque destabilization by regulating the behavior of endothelial cells. Moreover, it suggests that circRNA‑0006896 may represent a therapeutic target for controlling JNK/STAT3 signaling in HUVECs. Thus, this study may provide insight on potential interventions against vulnerable plaque formation in patients with AS.

/pdf/circrna-0006896-mir1264-dnmt1-axis-plays-an-important-role-4n0s0r8n8o.pdf

circRNA‑0006896‑miR1264‑DNMT1 axis plays an important role in carotid plaque destabilization by regulating the behavior of endothelial cells in atherosclerosis

Exosomes: An emerging factor in atherosclerosis

Corrigendum to "Exosomes: An emerging factor in atherosclerosis" [Biomed. Pharmacother. 115 (2019) 108951].

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Exosomes: An emerging factor in atherosclerosis

Corrigendum to "Exosomes: An emerging factor in atherosclerosis" [Biomed. Pharmacother. 115 (2019) 108951].