The role of extracellular vesicles in neointima formation post vascular injury

Pashova, A.; Work, Lorraine M.; Nicklin, SA

doi:10.1016/j.cellsig.2020.109783

Cited by 15 publications

(6 citation statements)

References 172 publications

(230 reference statements)

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“…Exosomes containing miRNA have recently emerged as important players in the intercellular communication between ECs and VSMCs (Hergenreider et al, 2012;Zheng et al, 2017). The ability to control restenosis with miRNAs through the use of exosomes is gaining interest (Pashova et al, 2020), but the exact mechanisms, such as the involvement of hnRNPs, are not clearly understood (Huber and Holvoet, 2015;Kapustin and Shanahan, 2016;Mukherjee et al, 2016). In this study, we investigated the ability of exosomes to mediate the delivery of miR-185 from VSMCs to ECs and assessed their effects on endothelialization after vascular injury.…”

Section: Discussionmentioning

confidence: 99%

Exosomal Transfer of miR-185 Is Controlled by hnRNPA2B1 and Impairs Re-endothelialization After Vascular Injury

Liu

Wang

et al. 2021

Front. Cell Dev. Biol.

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Dysfunction of endothelial cells (ECs) contributes to restenosis after vascular reconstruction for patients with coronary artery disease (CAD). The intercellular communication between ECs and vascular smooth muscle cells (VSMCs) might be critical in the development of restenosis and can be mediated by exosomes carrying functional microRNAs. miR-185 is reported to be associated with atherosclerosis, whether it plays a similar role in restenosis is unknown. In this study, we observed an elevated level of extracellular miR-185 in platelet-derived growth factor (PDGF)-stimulated VSMCs. The medium from PDGF-stimulated VSMCs promoted miR-185 expression in rat aortic ECs and inhibited EC angiogenesis. PDGF-stimulated VSMCs transferred miR-185 into ECs via exosomes. Furthermore, we found that the CXCL12 gene, a target of miR-185, is essential for the angiogenic potential of ECs. Exosomes derived from miR-185 mimic transfected VSMCs attenuated re-endothelialization after vascular injury. Moreover, we show that exosome-mediated miR-185 transfer is modulated by hnRNPA2B1. We also observed that hnRNPA2B1 is up-regulated during neointima formation and hnRNPA2B1 inhibition accelerates re-endothelialization and attenuates neointima formation following carotid injury. Taken together, our results indicate that exosomal miR-185 transfer from VSMCs to ECs is controlled by hnRNPA2B1 and impairs re-endothelialization after vascular injury.

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Section: Discussionmentioning

confidence: 99%

Exosomal Transfer of miR-185 Is Controlled by hnRNPA2B1 and Impairs Re-endothelialization After Vascular Injury

Liu

Wang

et al. 2021

Front. Cell Dev. Biol.

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“…Antiinflammatory effects mediated by BiNP-associated miR-451a could be beneficial for prevention of ischemia-reperfusion injury of organs, including donor organs used for transplantation [12]. Other potential clinical applications include attenuation of neointimal formation after vascular injury to prevent in-stent restenosis, and other occlusive vascular diseases [68]. The results of this study warrant further investigation into miR-451a as a mediator of immunomodulatory effects of adipose tissue BiNPs.…”

Section: Discussionmentioning

confidence: 77%

Effects of Adipose-Derived Biogenic Nanoparticle-Associated microRNA-451a on Toll-like Receptor 4-Induced Cytokines

Wang

Pham

et al. 2021

Pharmaceutics

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Extracellular vesicles (EVs) are cell-released nanoparticles that transfer biomolecular content between cells. Among EV-associated biomolecules, microRNAs (miRNAs/miRs) represent one of the most important modulators of signaling pathways in recipient cells. Previous studies have shown that EVs from adipose-derived mesenchymal stromal cells (MSCs) and adipose tissue modulate inflammatory pathways in macrophages. In this study, the effects of miRNAs that are abundant in adipose tissue EVs and other biogenic nanoparticles (BiNPs) were assessed in terms of altering Toll-like receptor 4 (TLR4)-induced cytokines. TLR-4 signaling in macrophages is often triggered by pathogen or damage-induced inflammation and is associated with several diseases. This study demonstrates that miR-451a, which is abundant in adipose tissue BiNPs, suppresses pro-inflammatory cytokines and increases anti-inflammatory cytokines associated with the TLR4 pathway. Therefore, miR-451a may be partially responsible for immunomodulatory effects of adipose tissue-derived BiNPs.

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“…Intimal hyperplasia is the pathological process that underlies arterial restenosis after endothelial damage, and it develops as a result of the migration of vascular smooth muscle cells (VSMCs) [1,2]. It is the main cause of vascular graft failure in the medium term [3][4][5]. A correct understanding of its molecular mechanisms and modulators may improve the outcomes of endovascular procedures.…”

Section: Introductionmentioning

confidence: 99%

Paricalcitol Has a Potent Anti-Inflammatory Effect in Rat Endothelial Denudation-Induced Intimal Hyperplasia

Baeza,

Pintor-Chocano,

Carrasco

et al. 2024

IJMS

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Neointimal hyperplasia is the main cause of vascular graft failure in the medium term. Vitamin D receptor activation modulates the biology of vascular smooth muscle cells and has been reported to protect from neointimal hyperplasia following endothelial injury. However, the molecular mechanisms are poorly understood. We have now explored the impact of the selective vitamin D receptor activator, paricalcitol, on neointimal hyperplasia, following guidewire-induced endothelial cell injury in rats, and we have assessed the impact of paricalcitol or vehicle on the expression of key cell stress factors. Guidewire-induced endothelial cell injury caused neointimal hyperplasia and luminal stenosis and upregulated the expression of the growth factor growth/differentiation factor-15 (GDF-15), the cytokine receptor CD74, NFκB-inducing kinase (NIK, an upstream regulator of the proinflammatory transcription factor NFκB) and the chemokine monocyte chemoattractant protein-1 (MCP-1/CCL2). Immunohistochemistry confirmed the increased expression of the cellular proteins CD74 and NIK. Paricalcitol (administered in doses of 750 ng/kg of body weight, every other day) had a non-significant impact on neointimal hyperplasia and luminal stenosis. However, it significantly decreased GDF-15, CD74, NIK and MCP-1/CCL2 mRNA expression, which in paricalcitol-injured arteries remained within the levels found in control vehicle sham arteries. In conclusion, paricalcitol had a dramatic effect, suppressing the stress response to guidewire-induced endothelial cell injury, despite a limited impact on neointimal hyperplasia and luminal stenosis. This observation identifies novel molecular targets of paricalcitol in the vascular system, whose differential expression cannot be justified as a consequence of improved tissue injury.

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The role of extracellular vesicles in neointima formation post vascular injury

Cited by 15 publications

References 172 publications

Exosomal Transfer of miR-185 Is Controlled by hnRNPA2B1 and Impairs Re-endothelialization After Vascular Injury

Exosomal Transfer of miR-185 Is Controlled by hnRNPA2B1 and Impairs Re-endothelialization After Vascular Injury

Effects of Adipose-Derived Biogenic Nanoparticle-Associated microRNA-451a on Toll-like Receptor 4-Induced Cytokines

Paricalcitol Has a Potent Anti-Inflammatory Effect in Rat Endothelial Denudation-Induced Intimal Hyperplasia

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