Plasma Small Extracellular Vesicle‐Carried miRNA‐501‐5p Promotes Vascular Smooth Muscle Cell Phenotypic Modulation‐Mediated In‐Stent Restenosis

Gao, Xiaofei; Wang, Zhimei; Chen, Ai-Qun; Wang, Feng; Luo, Shuai; Gu, Yue; Kong, Xiangquan; Zuo, Guang-Feng; Jiang, Xiaoyu; Ding, Guan-Wen; Chang, Yan; Ge, Zhen; Zhang, Junjie; Chen, Shao‐Liang

doi:10.1155/2021/6644970

Cited by 9 publications

(5 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…EVs bearing Ras-related protein 1 from patients with metabolic syndrome favored VSMC migration and proliferation [ 152 ]. Plasma EV containing miRNA-501-5p promotes VSMC phenotypic modulation through targeting Suppressor of mothers against decapentaplegic homolog (Smad) 3 in patients with in-stent restenosis one year after coronary stent implantation [ 153 ]. Conversely, several studies emphasize the fact that EVs and their miRNA content present an atheroprotective effect on VSMCs.…”

Section: Evs As Pathophysiological Drivers Of Atherothrombosismentioning

confidence: 99%

Extracellular Vesicles as Drivers of Immunoinflammation in Atherothrombosis

Suades

Greco

Padró

et al. 2022

Cells

View full text Add to dashboard Cite

Atherosclerotic cardiovascular disease is the leading cause of morbidity and mortality all over the world. Extracellular vesicles (EVs), small lipid-bilayer membrane vesicles released by most cellular types, exert pivotal and multifaceted roles in physiology and disease. Emerging evidence emphasizes the importance of EVs in intercellular communication processes with key effects on cell survival, endothelial homeostasis, inflammation, neoangiogenesis, and thrombosis. This review focuses on EVs as effective signaling molecules able to both derail vascular homeostasis and induce vascular dysfunction, inflammation, plaque progression, and thrombus formation as well as drive anti-inflammation, vascular repair, and atheroprotection. We provide a comprehensive and updated summary of the role of EVs in the development or regression of atherosclerotic lesions, highlighting the link between thrombosis and inflammation. Importantly, we also critically describe their potential clinical use as disease biomarkers or therapeutic agents in atherothrombosis.

show abstract

Section: Evs As Pathophysiological Drivers Of Atherothrombosismentioning

confidence: 99%

Extracellular Vesicles as Drivers of Immunoinflammation in Atherothrombosis

Suades

Greco

Padró

et al. 2022

Cells

View full text Add to dashboard Cite

show abstract

“…16) Currently recognized reasons for ISR are the hyper-proliferation and deposition of ECM in VSMCs. 17) Therefore, research on the migration, phenotypic transformation, and proliferation of VSMCs may shed novel light on promising therapeutic targets of ISR. In this context, this research intended to explore the mechanism of miR-22-3p in VSMC proliferation, phenotypic transformation, and migration.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-22-3p Restrains the Proliferation, Phenotypic Transformation, and Migration of Vascular Smooth Muscle Cells by Manipulating TOMM40

Tan

Yang

Bao³

et al. 2022

Int. Heart J.

View full text Add to dashboard Cite

microRNA (miR)-22-3p has been confirmed to be engaged in the phenotype transformation and proliferation of vascular smooth muscle cells (VSMCs), which is intimately correlated with restenosis. The current research set out to explore the detailed mechanism and function of miR-22-3p in VSMC proliferation, phenotype transformation, and migration via the translocase of outer mitochondrial membrane (TOMM40). Peripheral blood samples were acquired from patients with in-stent restenosis (ISR) after percutaneous coronary intervention (PCI), with subsequent quantitative reverse transcription (qRT)-polymerase chain reaction (PCR) and Western blot analyses of miR-22-3p and TOMM40 expression. After miR-22-3p-inhibitor, oe-TOMM40, and sh-TOMM40 were transfected into VSMCs, Cell Counting Kit (CCK)-8 assay, scratch test, and Western blot analysis were implemented to measure the VSMC proliferation, migration, and matrix metallopeptidase 9 (MMP9), α-smooth muscle actin (SMA), smooth muscle-myosin heavy chain (SM-MHC), and osteopontin (OPN) expressions, respectively. In addition, human umbilical vein endothelial cell (HUVEC) proliferation was examined by CCK-8 assay. The binding relationship between miR-22-3p and TOMM40 was assessed by dual luciferase reporter and RNA immunoprecipitation assays. The peripheral blood of patients with ISR after PCI had low expression of miR-22-3p and high expression of TOMM40. The mechanistic analysis reported the negative targeting relationship between miR-22-3p and TOMM40. Down-regulating miR-22-3p or up-regulating TOMM40 elevated the proliferation, migration, and phenotype transformation of VSMCs. miR-22-3p inhibitor had no evident impact on HUVEC proliferation. In addition, rescue assays displayed that TOMM40 silencing annulled miR-22-3p inhibition-enhanced VSMC proliferation, migration, and phenotype transformation. Conclusively, miR-22-3p could repress VSMC proliferation, phenotypic transformation, and migration by targeting TOMM40, which might be a possible treatment candidate for restenosis after PCI in patients with cardiovascular disease.

show abstract

“…RNases are capable of hydrolyzing Ex-ncRNAs. In linear ncRNAs, such as small and lncNRAs, RNase digestion can inhibit the development of arterial inflammation and suppress atherosclerosis [ 86 ]. Investigations on RNase-based therapies targeting Ex-ncRNAs have begun to reveal yet another critical avenue of ncRNA therapeutics [ 87 ].…”

Section: Ex-ncrnas As Therapeutic Targets In Cvdsmentioning

confidence: 99%

Extracellular Non-Coding RNAs in Cardiovascular Diseases

Jiapaer

Yang

et al. 2023

Pharmaceutics

View full text Add to dashboard Cite

Cardiovascular diseases (CVDs) remain the world’s leading cause of death despite the best available healthcare and therapy. Emerging as a key mediator of intercellular and inter-organ communication in CVD pathogenesis, extracellular vesicles (EVs) are a heterogeneous group of membrane-enclosed nano-sized vesicles released by virtually all cells, of which their RNA cargo, especially non-coding RNAs (ncRNA), has been increasingly recognized as a promising diagnostic and therapeutic target. Recent evidence shows that ncRNAs, such as small ncRNAs, circular RNAs, and long ncRNAs, can be selectively sorted into EVs or other non-vesicular carriers and modulate various biological processes in recipient cells. In this review, we summarize recent advances in the literature regarding the origin, extracellular carrier, and functional mechanisms of extracellular ncRNAs with a focus on small ncRNAs, circular RNAs, and long ncRNAs. The pathophysiological roles of extracellular ncRNAs in various CVDs, including atherosclerosis, ischemic heart diseases, hypertension, cardiac hypertrophy, and heart failure, are extensively discussed. We also provide an update on recent developments and challenges in using extracellular ncRNAs as biomarkers or therapeutical targets in these CVDs.

show abstract

Plasma Small Extracellular Vesicle‐Carried miRNA‐501‐5p Promotes Vascular Smooth Muscle Cell Phenotypic Modulation‐Mediated In‐Stent Restenosis

Cited by 9 publications

References 31 publications

Extracellular Vesicles as Drivers of Immunoinflammation in Atherothrombosis

Extracellular Vesicles as Drivers of Immunoinflammation in Atherothrombosis

MicroRNA-22-3p Restrains the Proliferation, Phenotypic Transformation, and Migration of Vascular Smooth Muscle Cells by Manipulating TOMM40

Extracellular Non-Coding RNAs in Cardiovascular Diseases

Contact Info

Product

Resources

About