Exosomal Notch3 from high glucose-stimulated endothelial cells regulates vascular smooth muscle cells calcification/aging

Lin, Xiao; Li, Shuang; Wang, Yanjiao; Wang, Yi; Zhong, Jia‐Yu; He, Jieyu; Cui, Xing‐Jun; Zhan, Jicheng; Liu, You‐Shuo

doi:10.1016/j.lfs.2019.116582

Cited by 66 publications

(64 citation statements)

References 35 publications

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“…Exosomes are an extracellular vesicle that can be produced by various types of cells and serve as an important participant in intercellular communication by transporting a variety of bioactive materials (proteins, nucleic acids, etc.) to other cells under physiological and pathological conditions [7,10]. Recently, extracellular vesicle induced vascular medial calci cation was one of the mechanisms of accelerated vascular calci cation in patients with chronic kidney disease [19].…”

Section: Discussionmentioning

confidence: 99%

“…Numerous studies have reported that exosomes are usually regarded as mediator of cell to cell communication in physiological and pathological conditions, because of their variety and the abundance of speci c cargos including proteins, lipids, and nucleic acids [6][7][8]. Recently,increasing evidence has shown that exosomes also play an important role in regulating vascular calci cation [9,10]. For instance Li et al reported that exosomes derived from high glucose induced endothelial cells could carry versican protein to accelerate VSMCs calci cation [9].…”

Section: Introductionmentioning

confidence: 99%

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Plasma exosomes derived from patients with end-stage renal disease and renal transplant recipients have different effects on vascular calcification

Lin

Zhu²,

Xing³

et al. 2020

Preprint

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Background End-stage renal disease (ESRD) patients usually develop extensive and progressive vascular calcification, and lots of calcification inhibitors as well as pro-calcifying factors are involved in the process. However, the mechanisms of vascular calcification in ESRD patients are still ill-defined. Methods The participants in the study were selected at the Second Xiangya Hospital, Central South University, and the plasma exosomes derived from ESRD patients (ESRD-Ex), renal transplant recipients (RTR-Ex), and the normal health control group (Nor-Ex) were isolated by ExoQuick-TC kit. Transmission electron microscopy and molecular size analysis were used to assess the morphology and size of exosomes. Alizarin Red S staining was carried out to detect calcification of vascular smooth muscle cells (VSMCs). Protein levels of Fetuin-A, matrix gla protein (MGP), Annexin-A2, bone morphogenetic protein (BMP-2), and receptor activator for nuclear factor-κ B ligand (Rankl) were measured by Western Blot analysis and the contents of that were detected using ELISA. Coronary artery calcification scores (CACS) were quantified via Agaston and analysed by Siemens CaScoring software. Results Compared with Nor-Ex, the ESRD-Ex promoted calcification of VSMCs significantly, and RTR-Ex could attenuate VSMCs calcification. Moreover, the protein concentration of ESRD-Ex was significantly higher than Nor-Ex and RTR-Ex, and the content of both MGP and Fetuin-A, the calcification inhibitors, were prominently lower in ESRD-Ex than those in Nor-Ex. The content of Annexin-A2, one of the calcification promoters, was significantly higher in ESRD-Ex and RTR-Ex than that in Nor-Ex. But, BMP-2 and Rankl had no significant difference among the three groups. In addition, the content of Fetuin-A in RTR-Ex was higher than that in ESRD-Ex, though it was still lower than in Nor-Ex. Furthermore, the content of both plasma Fetuin-A and MGP were negatively while that of Annexin-A2 was negatively correlated to CACS. Conclusions These results indicated that ESRD-Ex significantly promoted VSMCs calcification while renal transplantation could partially attenuate the effect of exosomes. Fetuin-A and MGP were decreased but Annexin-A2 was increased in ESRD-Ex, and renal transplantation could increase the level of Fetuin-A rather than MGP.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Plasma exosomes derived from patients with end-stage renal disease and renal transplant recipients have different effects on vascular calcification

Lin

Zhu²,

Xing³

et al. 2020

Preprint

Self Cite

View full text Add to dashboard Cite

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“…Moreover, TNF-α stimulation of HUVEC caused changes in EVs protein [163,[166][167][168][169], and microRNA expression [168][169][170]. These changes induced functional alterations in the recipient cells, suggesting that EC-derived EVs have a vital mediator role in CV homeostasis [140,[163][164][165][166][167][168][169][170].…”

Section: Extracellular Vesiclesmentioning

confidence: 99%

“…HUVEC have been used to evaluate how different stress conditions affect EVs composition, production, or content, as well as their communication with other endothelial or other cell types [5,[161][162][163][164]]. HUVEC exposed to high glucose concentrations increased EMV production and induced changes in their composition and functionality [162,165], contributing to endothelial dysfunction development and progression. Moreover, TNF-α stimulation of HUVEC caused changes in EVs protein [163,[166][167][168][169], and microRNA expression [168][169][170].…”

Section: Extracellular Vesiclesmentioning

confidence: 99%

Use of Human Umbilical Vein Endothelial Cells (HUVEC) as a Model to Study Cardiovascular Disease: A Review

et al. 2020

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Cardiovascular disease (CVD) is the leading cause of death worldwide, and extensive research has been performed to understand this disease better, using various experimental models. The endothelium plays a crucial role in the development of CVD, since it is an interface between bloodstream components, such as monocytes and platelets, and other arterial wall components. Human umbilical vein endothelial cell (HUVEC) isolation from umbilical cord was first described in 1973. To date, this model is still widely used because of the high HUVEC isolation success rate, and because HUVEC are an excellent model to study a broad array of diseases, including cardiovascular and metabolic diseases. We here review the history of HUVEC isolation, the HUVEC model over time, HUVEC culture characteristics and conditions, advantages and disadvantages of this model and finally, its applications in the area of cardiovascular diseases.

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“…Smoking induces DNA damage in a manner similar to obesity, which can aggravate senescence and trigger inflammation through the cGAS/STING pathway [154], and a sedentary lifestyle is associated with increased inflammation and oxidative stress [155]. In a high-glucose microenvironment, circulating EPCs, ECs and VSMCs undergo a decrease in telomerase activity and cellular senescence, and the control of blood glucose is an important strategy for controlling the risk factors of cellular senescence [135,156]. Insufficient sleep can lead to shortened telomeres and a significant increase in specific DNA damage, the accumulation of free radicals and the production of SASP factors in mice [157].…”

Section: Treatment Strategies Targeting Senescencementioning

confidence: 99%

Cellular Senescence Affects Cardiac Regeneration and Repair in Ischemic Heart Disease

Yan¹,

Xu²,

Huang³

2021

Aging and disease

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Ischemic heart disease (IHD) is defined as a syndrome of ischemic cardiomyopathy. Myogenesis and angiogenesis in the ischemic myocardium are important for cardiomyocyte (CM) survival, improving cardiac function and decreasing the progression of heart failure after IHD. Cellular senescence is a state of permanent irreversible cell cycle arrest caused by stress that results in a decline in cellular functions, such as proliferation, migration, homing, and differentiation. In addition, senescent cells produce the senescence-associated secretory phenotype (SASP), which affects the tissue microenvironment and surrounding cells by secreting proinflammatory cytokines, chemokines, growth factors, and extracellular matrix degradation proteins. The accumulation of cardiovascular-related senescent cells, including vascular endothelial cells (VECs), vascular smooth muscle cells (VSMCs), CMs and progenitor cells, is an important risk factor of cardiovascular diseases, such as vascular aging, atherosclerotic plaque formation, myocardial infarction (MI) and ventricular remodeling. This review summarizes the processes of angiogenesis, myogenesis and cellular senescence after IHD. In addition, this review focuses on the relationship between cellular senescence and cardiovascular disease and the mechanism of cellular senescence. Finally, we discuss a potential therapeutic strategy for MI targeting senescent cells.

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Exosomal Notch3 from high glucose-stimulated endothelial cells regulates vascular smooth muscle cells calcification/aging

Cited by 66 publications

References 35 publications

Plasma exosomes derived from patients with end-stage renal disease and renal transplant recipients have different effects on vascular calcification

Plasma exosomes derived from patients with end-stage renal disease and renal transplant recipients have different effects on vascular calcification

Use of Human Umbilical Vein Endothelial Cells (HUVEC) as a Model to Study Cardiovascular Disease: A Review

Cellular Senescence Affects Cardiac Regeneration and Repair in Ischemic Heart Disease

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