Vascular Smooth Muscle Cell Neutral Sphingomyelinase 2 in the Release of Exosomes and Vascular Calcification

Pavlic, Angelina; Sangani, Nasim Bahram; Kerins, Johanna; Nicolaes, Gerry A. F.; Schurgers, Leon J.; Reutelingsperger, Chris

doi:10.3390/ijms23169178

Cited by 9 publications

(6 citation statements)

References 105 publications

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“…In this study, we demonstrated that muscle cell-derived exosomes induced the neurite outgrowth in neuronal cells. Although there have been studies on the effects of adipocyte-derived exosomes on skeletal muscle [ 23 ] and the involvement of exosomes in muscle–kidney interactions [ 24 ], there are few reports on the functionality of exosomes produced by muscle cells [ 25 ]. In particular, results so far suggest that carnosine may induce the interaction between intestinal cells, muscle cells and neuronal cells via exosomes.…”

Section: Discussionmentioning

confidence: 99%

Molecular Mechanisms for the Carnosine-Induced Activation of Muscle–Brain Interaction

et al. 2023

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Carnosine is known to improve brain function. The molecular basis for the carnosine-mediated interaction between intestinal cells and neuronal cells is that carnosine acts on intestinal cells and stimulates exosome secretion, which can induce neurite outgrowth in neuronal cells. This study aimed to infer the carnosine-mediated interaction between muscle cells and neuronal cells. The results revealed that carnosine induces muscle cell differentiation, as well as the secretion of exosomes and myokines that can act on neuronal cells. Carnosine acts not only on intestinal cells but also on muscle cells, stimulating the secretion of secretory factors including exosomes that induce neurite outgrowth in neuronal cells, as well as myokines known to be involved in neuronal cell activation. As the miRNAs in exosomes secreted from intestinal cells and muscle cells upon carnosine treatment are different, it could be assumed that carnosine acts on each cell to interact with neuronal cell through separate factors and mechanisms.

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Section: Discussionmentioning

confidence: 99%

Molecular Mechanisms for the Carnosine-Induced Activation of Muscle–Brain Interaction

et al. 2023

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“…Phingomyelin phosphodiesterase 3 (SMPD3, also known as Neutral sphingomyelinase 2,nSM2) has been shown to regulate the release of exosomes [ 228 ]. Increased SMPD3 expression under high extracellular calcium promotes the secretion of calcifying exosomes [ 17 ], and inhibition of SMPD3 expression by Barley-ß-glucans prevents VSMC calcification [ 229 ].…”

Section: The Crosstalk In Vascular Calcificationmentioning

confidence: 99%

Vascular calcification: from the perspective of crosstalk

Yang,

Zeng,

Yuan

et al. 2023

Mol Biomed

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Vascular calcification (VC) is highly correlated with cardiovascular disease morbidity and mortality, but anti-VC treatment remains an area to be tackled due to the ill-defined molecular mechanisms. Regardless of the type of VC, it does not depend on a single cell but involves multi-cells/organs to form a complex cellular communication network through the vascular microenvironment to participate in the occurrence and development of VC. Therefore, focusing only on the direct effect of pathological factors on vascular smooth muscle cells (VSMCs) tends to overlook the combined effect of other cells and VSMCs, including VSMCs-VSMCs, ECs-VMSCs, Macrophages-VSMCs, etc. Extracellular vesicles (EVs) are a collective term for tiny vesicles with a membrane structure that are actively secreted by cells, and almost all cells secrete EVs. EVs docked on the surface of receptor cells can directly mediate signal transduction or transfer their contents into the cell to elicit a functional response from the receptor cells. They have been proven to participate in the VC process and have also shown attractive therapeutic prospects. Based on the advantages of EVs and the ability to be detected in body fluids, they may become a novel therapeutic agent, drug delivery vehicle, diagnostic and prognostic biomarker, and potential therapeutic target in the future. This review focuses on the new insight into VC molecular mechanisms from the perspective of crosstalk, summarizes how multi-cells/organs interactions communicate via EVs to regulate VC and the emerging potential of EVs as therapeutic methods in VC. We also summarize preclinical experiments on crosstalk-based and the current state of clinical studies on VC-related measures.

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“…Phenotypic conversion of VSMC is a key aspect of VC development. VSMC can be converted from a contractile phenotype to a synthetic phenotype, facilitating the release of EVs and converting them to a calcified state ( 37 ). Calcified EVs contain fewer inhibitors of calcification, and when released into the ECM, it tends to aggregate and form microcalcifications in areas of sparse collagen.…”

Section: Extracellular Vesiclesmentioning

confidence: 99%

The role of extracellular vesicles in vascular calcification in chronic kidney disease

Zhao

Liu²,

Liu³

et al. 2022

Front. Med.

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Widespread vascular calcification (VC) in patients with chronic kidney disease (CKD) is the pathological basis for the development of cardiovascular disease, and VC has been identified as an independent risk factor for increased cardiovascular mortality in cases of CKD. While VC was earlier thought to be a passive deposition process following calcium and phosphorus supersaturation, recent studies have suggested that it is an active, modifiable, biological process similar to bone development. The involvement of extracellular vesicles (EVs) in the process of VC has been reported as an important transporter of material transport and intercellular communication. This paper reviews the mechanism of the role of EVs, especially exosomes, in VC and the regulation of VC by stem cell-derived EVs, and discusses the possible and promising application of related therapeutic targets in the clinical setting.

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Vascular Smooth Muscle Cell Neutral Sphingomyelinase 2 in the Release of Exosomes and Vascular Calcification

Cited by 9 publications

References 105 publications

Molecular Mechanisms for the Carnosine-Induced Activation of Muscle–Brain Interaction

Molecular Mechanisms for the Carnosine-Induced Activation of Muscle–Brain Interaction

Vascular calcification: from the perspective of crosstalk

The role of extracellular vesicles in vascular calcification in chronic kidney disease

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