Nitric oxide improves regeneration and prevents calcification in bio-hybrid vascular grafts via regulation of vascular stem/progenitor cells

Wang, Fei; Qin, Kang; Wang, Kai; Wang, He; Liu, Qi; Qian, Meng; Chen, Shang; Sun, Yuting; Hou, Jingli; Wei, Yongzhen; Hu, Yanhua; Li, Zongjin; Xu, Qingbo; Zhao, Qiang

doi:10.1016/j.celrep.2022.110981

Cited by 19 publications

(9 citation statements)

References 72 publications

(88 reference statements)

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“…Effectively targeting and regulating the differentiation of Gli1 + cells is the key goal of this study. Previous studies focused on the regulation of graft environment, such as modifying antioxidant substances ( 32 ) or nitric oxide (NO)–releasing molecules on TEBVs ( 9 ), achieving anticalcification through antioxidant effect, or using the immunomodulatory effect of MSC-EXO to prevent calcification ( 37 ), but these studies did not eliminate the symptoms of vascular calcification from the source. Exosome is the key bridge of intercellular communication, which can be used for signal transmission such as RNA.…”

Section: Discussionmentioning

confidence: 99%

“…However, when TEBVs are implanted into patients with underlying diseases such as diabetes, calcification is also easy to occur in grafts and leads to implantation failure ( 7 ). For TEBVs, on the one hand, it is necessary to promote the rapid and normal reconstruction of SMCs to resist the occurrence of aneurysms ( 8 ); on the other hand, it is necessary to inhibit calcification to maintain long-term homeostasis and vascular patency ( 3 , 9 ). At present, there is no noninvasive treatment for vascular calcification under the above pathological conditions.…”

Section: Introductionmentioning

confidence: 99%

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Engineered exosomes reprogram Gli1 ⁺ cells in vivo to prevent calcification of vascular grafts and autologous pathological vessels

et al. 2023

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Calcification of autologous pathological vessels and tissue engineering blood vessels (TEBVs) is a thorny problem in clinic. However, there is no effective and noninvasive treatment that is available against the calcification of TEBVs and autologous pathological vessels. Gli1 + cells are progenitors of smooth muscle cells (SMCs) and can differentiate into osteoblast-like cells, leading to vascular calcification. Our results showed that the spatiotemporal distribution of Gli1 + cells in TEBVs was positively correlated with the degree of TEBV calcification. An anticalcification approach was designed consisting of exosomes derived from mesenchymal stem cells delivering lncRNA-ANCR to construct the engineered exosome-Ancr/E7-EXO. The results showed that Ancr/E7-EXO effectively targeted Gli1 + cells, promoting rapid SMC reconstruction and markedly inhibiting Gli1 + cell differentiation into osteoblast-like cells. Moreover, Ancr/E7-EXO significantly inhibited vascular calcification caused by chronic kidney disease. Therefore, Ancr/E7-EXO reprogrammed Gli1 + cells to prevent calcification of vascular graft and autologous pathological vessel, providing unique insights for an effective anticalcification.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Engineered exosomes reprogram Gli1 ⁺ cells in vivo to prevent calcification of vascular grafts and autologous pathological vessels

et al. 2023

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“…NO can also inhibit the proliferation and migration of vascular smooth muscle cells, promote the proliferation and migration of endothelial cells, and suppress endothelial cell apoptosis [ 34 , 35 , 36 ]. NO plays a role in promoting vascular regeneration and inhibiting vascular calcification by regulating the differentiation of endogenous vascular stem/progenitor cells into vascular endothelial cells and inhibiting their osteogenic differentiation [ 37 ]. These results suggest the specific effects of NO depend on the context and the type of cells involved, and dysregulation of NO signaling can contribute to a variety of neurological and psychiatric disorders.…”

Section: Discussionmentioning

confidence: 99%

The Inhibition Effects of Sodium Nitroprusside on the Survival of Differentiated Neural Stem Cells through the p38 Pathway

Jiao

et al. 2023

Brain Sciences

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Nitric oxide (NO) is a crucial factor in regulating neuronal development. However, certain effects of NO are complex under different physiological conditions. In this study, we used differentiated neural stem cells (NSCs), which contained neural progenitor cells, neurons, astrocytes, and oligodendrocytes, to observe the physiological effects of sodium nitroprusside (SNP) on the early developmental stage of the nervous system. After SNP treatment for 24 h, the results showed that SNP at 100 μM, 200 μM, 300 μM, and 400 μM concentrations resulted in reduced cell viability and increased cleaved caspase 3 levels, while no significant changes were found at 50 μM. There were no effects on neuronal differentiation in the SNP-treated groups. The phosphorylation of p38 was also significantly upregulated with SNP concentrations of 100 μM, 200 μM, 300 μM, and 400 μM, with no changes for 50 μM concentration in comparison with the control. We also observed that the levels of phosphorylation increased with the increasing concentration of SNP. To further explore the possible role of p38 in SNP-regulated survival of differentiated NSCs, SB202190, the antagonist of p38 mitogen-activated protein kinase, at a concentration of 10 mM, was pretreated for 30 min, and the ratio of phosphorylated p38 was found to be decreased after treatment with SNP. Survival and cell viability increased in the SB202190 and SNP co-treated group. Taken together, our results suggested that p38 is involved in the cell survival of NSCs, regulated by NO.

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“…Hu et al investigated hybrid grafts with poly (lactide-co-epsilon-caprolactone) (PLCL), collagen, and elastin loaded with heparin and VEGF in a short-term animal study (rabbit model, follow-up of 28 days), which showed increased cell adhesion and a high EC proliferation rate ( 87 ). Similarly, Wang et al reported enhanced vascular regeneration and inhibition of intimal hyperplasia and vascular calcification after implantation of bio-hybrid vascular grafts with local NO delivery in both rabbit and mouse models ( 88 ). In another large animal study (sheep model), an acellular tissue engineered vessel based on small intestinal submucosa functionalized with heparin and VEGF demonstrated impressive mechanical properties with concomitant successful endothelialization ( 89 ).…”

Section: Endothelialization Of Vascular Graftsmentioning

confidence: 95%

The path to a hemocompatible cardiovascular implant: Advances and challenges of current endothelialization strategies

Exarchos

Zacharova

Neuber

et al. 2022

Front. Cardiovasc. Med.

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Cardiovascular (CV) implants are still associated with thrombogenicity due to insufficient hemocompatibility. Endothelialization of their luminal surface is a promising strategy to increase their hemocompatibility. In this review, we provide a collection of research studies and review articles aiming to summarize the recent efforts on surface modifications of CV implants, including stents, grafts, valves, and ventricular assist devises. We focus in particular on the implementation of micrometer or nanoscale surface modifications, physical characteristics of known biomaterials (such as wetness and stiffness), and surface morphological features (such as gratings, fibers, pores, and pits). We also review how biomechanical signals originating from the endothelial cell for surface interaction can be directed by topography engineering approaches toward the survival of the endothelium and its long-term adaptation. Finally, we summarize the regulatory and economic challenges that may prevent clinical implementation of endothelialized CV implants.

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Nitric oxide improves regeneration and prevents calcification in bio-hybrid vascular grafts via regulation of vascular stem/progenitor cells

Cited by 19 publications

References 72 publications

Engineered exosomes reprogram Gli1 ⁺ cells in vivo to prevent calcification of vascular grafts and autologous pathological vessels

Engineered exosomes reprogram Gli1 ⁺ cells in vivo to prevent calcification of vascular grafts and autologous pathological vessels

The Inhibition Effects of Sodium Nitroprusside on the Survival of Differentiated Neural Stem Cells through the p38 Pathway

The path to a hemocompatible cardiovascular implant: Advances and challenges of current endothelialization strategies

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Nitric oxide improves regeneration and prevents calcification in bio-hybrid vascular grafts via regulation of vascular stem/progenitor cells

Cited by 19 publications

References 72 publications

Engineered exosomes reprogram Gli1 + cells in vivo to prevent calcification of vascular grafts and autologous pathological vessels

Engineered exosomes reprogram Gli1 + cells in vivo to prevent calcification of vascular grafts and autologous pathological vessels

The Inhibition Effects of Sodium Nitroprusside on the Survival of Differentiated Neural Stem Cells through the p38 Pathway

The path to a hemocompatible cardiovascular implant: Advances and challenges of current endothelialization strategies

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Engineered exosomes reprogram Gli1 ⁺ cells in vivo to prevent calcification of vascular grafts and autologous pathological vessels

Engineered exosomes reprogram Gli1 ⁺ cells in vivo to prevent calcification of vascular grafts and autologous pathological vessels