Extracellular vesicles as modifiers of epigenomic profiles

表观遗传学 表观遗传学 组蛋白 生物 细胞外小泡 生物发生 细胞生物学 胞外囊泡 非编码RNA 计算生物学 DNA甲基化 核糖核酸 小RNA 遗传学 DNA 微泡 基因表达 基因
作者
Haifeng Zhou,Sheng Hu,Wei Yan
出处
期刊:Trends in Genetics [Elsevier BV]
卷期号:40 (9): 797-809 被引量:4
标识
DOI:10.1016/j.tig.2024.05.005
摘要

Extracellular vesicles (EVs) and epigenomic profiles are closely linked and reciprocally regulated. EVs reprogram the epigenomic profile by remodeling DNA, RNA, and histone modifications in recipient cells, by delivering cargoes mainly targeting methyltransferase and demethyltransferase. EVs display great potential as diagnostic markers and epidrug delivery vehicles for therapeutic applications. Advanced technologies and multi-omic profiling to define single EV characterization would improve the loading efficacy and delivery accuracy of EVs in disease treatments. Extracellular vesicles (EVs), emerging as novel mediators between intercellular communication, encapsulate distinct bioactive cargoes to modulate multiple biological events, such as epigenetic remodeling. In essence, EVs and epigenomic profiles are tightly linked and reciprocally regulated. Epigenetic factors, including histone and DNA modifications, noncoding RNAs, and protein post-translational modifications (PTMs) dynamically regulate EV biogenesis to contribute to EV heterogeneity. Alternatively, EVs actively modify DNA, RNA, and histone profiles in recipient cells by delivering RNA and protein cargoes for downstream epigenetic enzyme regulation. Moreover, EVs display great potential as diagnostic markers and drug-delivery vehicles for therapeutic applications. The combination of parental cell epigenomic modification with single EV characterization would be a promising strategy for EV engineering to enhance the epidrug loading efficacy and accuracy. Extracellular vesicles (EVs), emerging as novel mediators between intercellular communication, encapsulate distinct bioactive cargoes to modulate multiple biological events, such as epigenetic remodeling. In essence, EVs and epigenomic profiles are tightly linked and reciprocally regulated. Epigenetic factors, including histone and DNA modifications, noncoding RNAs, and protein post-translational modifications (PTMs) dynamically regulate EV biogenesis to contribute to EV heterogeneity. Alternatively, EVs actively modify DNA, RNA, and histone profiles in recipient cells by delivering RNA and protein cargoes for downstream epigenetic enzyme regulation. Moreover, EVs display great potential as diagnostic markers and drug-delivery vehicles for therapeutic applications. The combination of parental cell epigenomic modification with single EV characterization would be a promising strategy for EV engineering to enhance the epidrug loading efficacy and accuracy. a kind of programmed cell death for orderly and efficient removal of damaged cells. centrosome relocation triggered by an external signal to define the polarity axis of the cell. the process of determining the nature of a disease or disorder based on a series of examinations for testing related marker level. drug that targets the enzymes essential for the maintenance and establishment of epigenetic modifications, with the main strategy of inhibiting DNA methyltransferases and histone deacetylases. a phenomenon that changes gene expression without any alteration of genetic sequence; plays an important role in multiple biological events during development and diseases. the process of modifying extracellular vesicles with surface decoration or loading luminal chemicals/molecules for therapeutic applications. a subset of smaller extracellular vesicles (40–160nm in diameter) with endosomal origin and defined by the subset of intraluminal vesicles that undergo secretion upon multivesicular body fusion with the plasma membrane, participating in cell–cell communication by delivering bioactive cargoes. heterogeneous populations of membrane vesicles that originated from the endosomal compartment or budding of the plasma membrane, encapsulating bioactive cargoes, including nucleic acids, proteins, and metabolites, to mediate cell–cell communication. actin-based structures that drive the proteolytic invasion of cells, by forming highly regulated platforms for the localized release of lytic enzymes that degrade the matrix. plasma membrane microdomains enriched in sphingolipids and cholesterol, participating in membrane domain heterogeneity, signaling, and membrane trafficking. a process of adding mineral to matrix in bone. intracellular endosomal organelle enclosed within a single outer membrane, containing intraluminal vesicles generated from invagination and budding of the membrane, either fused with lysosomes for degradation or released exosomes upon plasma membrane fusion. the uptake process of macromolecules and larger energy-rich particles into the cell. inflammasome-initiated lytic programmed cell death for detection of cytosolic contamination or perturbation.
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