Vascular tissue engineering: the next generation

Cleary, Muriel A.; Geiger, Erik J.; Grady, Conor; Best, Cameron; Naito, Yuji; Breuer, Christopher K.

doi:10.1016/j.molmed.2012.04.013

Cited by 135 publications

(112 citation statements)

References 80 publications

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“…5 Current research is aimed at identifying the underlying cellular and molecular mechanisms of vascular neotissue formation, TEVG remodeling upon scaffold degradation, and the development of TEVG stenosis to rationally design a second-generation TEVG with off-the-shelf availability for clinical translation. 2,6,7 The transition from biodegradable scaffold to vascular neotissue is an inflammation-mediated remodeling process dependent upon the activity of infiltrating host-derived monocytes and macrophages. 8,9 Paracrine signaling from inflammatory cells within the scaffold in the form of growth factors, cytokines, and chemokines induces migration of neighboring native smooth muscle and endothelial cells, which take residence in the scaffold and proliferate to form the medial and intimal layers of the neovessel as scaffold materials degrade.…”

Section: Introductionmentioning

confidence: 99%

Novel Association of miR-451 with the Incidence of TEVG Stenosis in a Murine Model

Hibino

Best

Engle

et al. 2016

Tissue Engineering Part A

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The development of a tissue-engineered vascular graft (TEVG) holds great promise for advancing the field of cardiac surgery. Despite the successful translation of this technology, previous reports identify the primary mode of graft failure as stenosis secondary to intimal hyperplasia. MicroRNAs (miRNAs) regulate gene expression by interfering with mRNA function and recent research has suggested miRNA as a potential therapeutic target. The role of miRNAs in TEVGs during neotissue formation is currently unknown. In this study, we investigated if miRNAs regulate the inhibition of graft stenosis. Biodegradable PGA-P(LA/CL) scaffolds were implanted as inferior vena cava interposition grafts in a murine model (n = 14). Mice were sacrificed 14 days following implantation and TEVGs were harvested for histological analysis and miRNA profiling using Affymetrix miRNA arrays. Graft diameters were measured histologically, and the largest grafts (patent group) and smallest grafts (stenosed group) were profiled (n = 4 for each group). Cell population in each graft was analyzed with immunohistochemistry using antismooth muscle actin (SMA) and antimacrophage (F4/ 80) antibodies. The graft diameter was significantly greater in the patent group (0.63 -0.06 mm) than in the stenosed group (0.17 -0.06 mm) ( p < 0.01). Cell proliferation was significantly greater in the stenosed grafts than in patent grafts ( p < 0. MiRNA array of 1416 genes showed that in stenosed grafts, mir-451, mir-338, and mir-466 were downregulated and mir-154 was upregulated. Mir-451 exhibited the greatest difference in expression between stenosed and patent grafts by -3.1-fold. Significant negative correlation was found between the expression of mir-451 and cell proliferation (SMA: r = -0.86, p = 0.003; F4/80: r = -0.89, p = 0.001). Our data, along with previous evidence that mir-451 regulates tumor suppressor genes, suggest that downregulation of mir-451 promotes acute proliferation of macrophages and smooth muscle cells, thereby inducing TEVG stenosis. Adequate expression of mir-451 may be critical for improving TEVG patency.

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Section: Introductionmentioning

confidence: 99%

Novel Association of miR-451 with the Incidence of TEVG Stenosis in a Murine Model

Hibino

Best

Engle

et al. 2016

Tissue Engineering Part A

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“…Doku oluumunu yönlendiren ve yeniden ekillendirmeye olanak sa¤layan biyolojik ve mekanik sinyallerdir. [6] Otolog doku oluturmak için öncelikle biyotasarım stratejileri, doku mühendisli¤i implantlarının uygulama potansiyeli kadar çeitlidir ve bu nedenle tek bir tartımada ele alınması zordur. Bu nedenle kardiyovasküler doku mühendisli¤i uygulama alanı, Kardiyomiyosit uygulaması, kan damarları ve kalp kapakçıkları uygulamaları açı-sından ele alınmaktadır.…”

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Cardiovascular tissue engineering: Approaches and preclinical applications

Erdal¹

2017

FNG & Bilim Tıp Transplantasyon Dergisi

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Currently, cardiovascular diseases are among the most common causes of death in adults, with high mortality rates. The treatment of cardiovascular diseases is limited by factors such as donor deficiency and immunological tolerance. On the face of it, studies on person-specific treatment methods are rapidly taking place. Tissue engineering studies are accelerating with the developments in biomaterials science and existing cell studies and applications. Tissue engineering approach in tissue damage treatment and cardiovascular applications also pioneer in terms of clinical applications. In this review, we explain, ongoing tissue applications and preclinical studies in cardiomyocyte and heart valve models treatment are described. Kard‹yovasKüler doKu Mühend‹sl‹⁄‹Doku mühendisli¤inin amacı, hasar görmü veya ilevini kaybetmi doku/organ yapılarının geometrisine özgü yeni doku iskeleleri üreterek vücuda uyumlu ve doku/organın ilevini yerine getirebilecek yapay doku oluturmaktır. [1,2] Kardiyovasküler fizyoloji açısından kardiyovaskü-ler doku mühendisli¤i, balangıçtan beri uygulama ve tedavi açısından doku mühendisli¤i çalımaları alanında öncelikli hedeflerden olmutur.Günümüzde, kardiyovasküler hastalıklar genel ölüm nedenlerinin %20'sini oluturur iken ve ABD'deki erikinlerde en sık rastlanan ölüm nedenidir.[3] Bu açıdan kardiyovasküler tedavi için önemli adımlar atılmı olmakla birlikte, protez implantlarının kullanılmasını gerektiren cerrahi müdahale birçok yetikin hastada kritik olmaya devam etmektedir. Buna ra¤men, kalp nakli, son dönem kalp yetmezli¤i için tek ve kesin tedavi olmaya devam etmektedir. Buna ek olarak, do¤utan kalp anomalileri, yenido¤an döneminde önde gelen ölüm nedenidir ve bu hasta nüfusunda

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“…Restoration of a functional pulmonary vasculature will require reestablishing intact, i.e., quiescent and nonthrombogenic, endothelial cell monolayers lining the entire vascular tree throughout the complex decellularized scaffold (17,95). We posit that successful bioengineering of functional lungs and their clinical usefulness will depend on innovative approaches to restoring a functional pulmonary vasculature.…”

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confidence: 99%