Vascular Smooth Muscle Cell-Derived Exosomal MicroRNAs Regulate Endothelial Cell Migration Under PDGF Stimulation

Heo, Jeongyeon; Yang, Hee Cheol; Rhee, Won Jong; Kang, Hyunjin

doi:10.3390/cells9030639

Cited by 32 publications

(16 citation statements)

References 42 publications

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“…BMP4 treatment increased miR-101 levels by approximately 5-fold ( Figure 2 A). miR-21 and miR-486, the miRNAs whose expression is stimulated by BMP signaling or platelet-derived growth factor (PDGF) signaling, respectively, were included as controls [ 21 , 27 ]. As expected, miR-21 levels were increased, while miR-486 levels were unaffected by BMP4 treatment.…”

Section: Resultsmentioning

confidence: 99%

BMP-Induced MicroRNA-101 Expression Regulates Vascular Smooth Muscle Cell Migration

Park

Kang

2020

IJMS

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Proliferation and migration of vascular smooth muscle cells (VSMCs) are implicated in blood vessel development, maintenance of vascular homeostasis, and pathogenesis of vascular disorders. MicroRNAs (miRNAs) mediate the regulation of VSMC functions in response to microenvironmental signals. Because a previous study reported that miR-101, a tumor-suppressive miRNA, is a critical regulator of cell proliferation in vascular disease, we hypothesized that miR-101 controls important cellular processes in VSMCs. The present study aimed to elucidate the effects of miR-101 on VSMC function and its molecular mechanisms. We revealed that miR-101 regulates VSMC proliferation and migration. We showed that miR-101 expression is induced by bone morphogenetic protein (BMP) signaling, and we identified dedicator of cytokinesis 4 (DOCK4) as a novel target of miR-101. Our results suggest that the BMP–miR-101–DOCK4 axis mediates the regulation of VSMC function. Our findings help further the understanding of vascular physiology and pathology.

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Section: Resultsmentioning

confidence: 99%

BMP-Induced MicroRNA-101 Expression Regulates Vascular Smooth Muscle Cell Migration

Park

Kang

2020

IJMS

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“…Similar results on endothelial migratory activity were described in artery endothelial cells (PAECs) exposed to PDGF stimulated VSMCs-derived exosomes. Downregulation of miR-1246, miR-182, and miR-486 in vascular smooth muscle´s exosomes promote endothelial migration [ 91 ]. Moreover, VSMCs secrete exosomes that promote vascular calcification under calcium stress triggers [ 92 , 93 ].…”

Section: Ec–vsmc Communicationmentioning

confidence: 99%

Cellular Crosstalk between Endothelial and Smooth Muscle Cells in Vascular Wall Remodeling

Méndez‐Barbero

Gutiérrez-Muñoz

Blanco-Colio

2021

IJMS

104

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Pathological vascular wall remodeling refers to the structural and functional changes of the vessel wall that occur in response to injury that eventually leads to cardiovascular disease (CVD). Vessel wall are composed of two major primary cells types, endothelial cells (EC) and vascular smooth muscle cells (VSMCs). The physiological communications between these two cell types (EC–VSMCs) are crucial in the development of the vasculature and in the homeostasis of mature vessels. Moreover, aberrant EC–VSMCs communication has been associated to the promotor of various disease states including vascular wall remodeling. Paracrine regulations by bioactive molecules, communication via direct contact (junctions) or information transfer via extracellular vesicles or extracellular matrix are main crosstalk mechanisms. Identification of the nature of this EC–VSMCs crosstalk may offer strategies to develop new insights for prevention and treatment of disease that curse with vascular remodeling. Here, we will review the molecular mechanisms underlying the interplay between EC and VSMCs. Additionally, we highlight the potential applicable methodologies of the co-culture systems to identify cellular and molecular mechanisms involved in pathological vascular wall remodeling, opening questions about the future research directions.

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“…VSMC-derived exosomes are novel critical regulators of vascular hemostasis 150 , 151 . miR-1246 , miR-182 , and miR-486 in VSMC-derived exosomes play essential roles in the maintenance of vascular homeostasis 152 . Numerous studies have shown that proliferation, phenotype switching (mainly contractile to migratory state), apoptosis, and calcification of VSMCs are closely linked to the onset and progression of atherosclerosis 153 - 155 .…”

Section: Exosomes In Atherogenesismentioning

confidence: 99%

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

et al. 2021

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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.

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Vascular Smooth Muscle Cell-Derived Exosomal MicroRNAs Regulate Endothelial Cell Migration Under PDGF Stimulation

Cited by 32 publications

References 42 publications

BMP-Induced MicroRNA-101 Expression Regulates Vascular Smooth Muscle Cell Migration

BMP-Induced MicroRNA-101 Expression Regulates Vascular Smooth Muscle Cell Migration

Cellular Crosstalk between Endothelial and Smooth Muscle Cells in Vascular Wall Remodeling

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

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