scholarly journals Additive Manufacturing of Nerve Decellularized Extracellular Matrix-Contained Polyurethane Conduits for Peripheral Nerve Regeneration

Polymers ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 1612 ◽  
Author(s):  
Chen ◽  
Chen ◽  
Ng ◽  
Lou ◽  
Chen ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Nerve Regeneration ◽  
Nerve Repair ◽  
Sensory Information ◽  
Cellular Adhesion ◽  
Electrical Signal ◽  
Potential Candidate ◽  
Body Parts ◽  
Digital Light Processing ◽  
Nerve Conduits

The nervous system is the part of our body that plays critical roles in the coordination of actions and sensory information as well as communication between different body parts through electrical signal transmissions. Current studies have shown that patients are likely to experience a functional loss if they have to go through a nerve repair for >15 mm lesion. The ideal treatment methodology is autologous nerve transplant, but numerous problems lie in this treatment method, such as lack of harvesting sites. Therefore, researchers are attempting to fabricate alternatives for nerve regeneration, and nerve conduit is one of the potential alternatives for nerve regeneration. In this study, we fabricated polyurethane/polydopamine/extracellular matrix (PU/PDA/ECM) nerve conduits using digital light processing (DLP) technology and assessed for its physical properties, biodegradability, cytocompatibility, neural related growth factor, and proteins secretion and expression and its potential in allowing cellular adhesion and proliferation. It was reported that PU/PDA/ECM nerve conduits were more hydrophilic and allowed enhanced cellular adhesion, proliferation, expression, and secretion of neural-related proteins (collagen I and laminin) and also enhanced expression of neurogenic proteins, such as nestin and microtubule-associated protein 2 (MAP2). In addition, PU/PDA/ECM nerve conduits were reported to be non-cytotoxic, had sustained biodegradability, and had similar physical characteristics as PU conduits. Therefore, we believed that PU/PDA/ECM nerve conduits could be a potential candidate for future nerve-related research or clinical applications.

scholarly journals Additive Manufacturing of Astragaloside-Containing Polyurethane Nerve Conduits Influenced Schwann Cell Inflammation and Regeneration

Processes ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 353
Author(s):  
Yueh-Sheng Chen ◽  
Shih-Sheng Chang ◽  
Hooi Yee Ng ◽  
Yu-Xuan Huang ◽  
Chien-Chang Chen ◽  
...  
Keyword(s):  
Nervous System ◽  
Cellular Proliferation ◽  
Neural Regeneration ◽  
Nerve Grafting ◽  
Necrosis Factor Alpha ◽  
Digital Light Processing ◽  
Nerve Conduits ◽  
Tnf Α ◽  
The Central Nervous System ◽  
Factor Alpha

The peripheral nervous system is the bridge of communication between the central nervous system and other body systems. Autologous nerve grafting is the mainstream method for repair of nerve lesions greater than 20 mm. However, there are several disadvantages and limitations of autologous nerve grafting, thus prompting the need for fabrication of nerve conduits for clinical use. In this study, we successfully fabricated astragaloside (Ast)-containing polyurethane (PU) nerve guidance conduits via digital light processing, and it was noted that the addition of Ast improved the hydrophilicity of traditional PU conduits by at least 23%. The improved hydrophilicity not only led to enhanced cellular proliferation of rat Schwann cells, we also noted that levels of inflammatory markers tumor necrosis factor-alpha (TNF-α) and cyclooxygenase-2 (COX-2) significantly decreased with increasing concentrations of Ast. Furthermore, the levels of neural regeneration markers were significantly enhanced with the addition of Ast. This study demonstrated that Ast-containing PU nerve conduits can be potentially used as an alternative solution to regenerate peripheral nerve injuries.

scholarly journals IL-17F depletion accelerates chitosan conduit guided peripheral nerve regeneration

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Feixiang Chen ◽  
Weihuang Liu ◽  
Qiang Zhang ◽  
Ping Wu ◽  
Ao Xiao ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Sciatic Nerve ◽  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Knockout Mice ◽  
Inflammatory Markers ◽  
Nerve Repair ◽  
Peripheral Nerve Regeneration ◽  
Wild Type ◽  
Anti Inflammatory

AbstractPeripheral nerve injury is a serious health problem and repairing long nerve deficits remains a clinical challenge nowadays. Nerve guidance conduit (NGC) serves as the most promising alternative therapy strategy to autografts but its repairing efficiency needs improvement. In this study, we investigated whether modulating the immune microenvironment by Interleukin-17F (IL-17F) could promote NGC mediated peripheral nerve repair. Chitosan conduits were used to bridge sciatic nerve defect in IL-17F knockout mice and wild-type mice with autografts as controls. Our data revealed that IL-17F knockout mice had improved functional recovery and axonal regeneration of sciatic nerve bridged by chitosan conduits comparing to the wild-type mice. Notably, IL-17F knockout mice had enhanced anti-inflammatory macrophages in the NGC repairing microenvironment. In vitro data revealed that IL-17F knockout peritoneal and bone marrow derived macrophages had increased anti-inflammatory markers after treatment with the extracts from chitosan conduits, while higher pro-inflammatory markers were detected in the Raw264.7 macrophage cell line, wild-type peritoneal and bone marrow derived macrophages after the same treatment. The biased anti-inflammatory phenotype of macrophages by IL-17F knockout probably contributed to the improved chitosan conduit guided sciatic nerve regeneration. Additionally, IL-17F could enhance pro-inflammatory factors production in Raw264.7 cells and wild-type peritoneal macrophages. Altogether, IL-17F may partially mediate chitosan conduit induced pro-inflammatory polarization of macrophages during nerve repair. These results not only revealed a role of IL-17F in macrophage function, but also provided a unique and promising target, IL-17F, to modulate the microenvironment and enhance the peripheral nerve regeneration.

PLGA artificial nerve conduits with dental pulp cells promote facial nerve regeneration

2011 ◽  
Vol 5 (10) ◽  
pp. 823-830 ◽  
Author(s):  
Ryo Sasaki ◽  
Shunsuke Aoki ◽  
Masayuki Yamato ◽  
Hiroto Uchiyama ◽  
Keiji Wada ◽  
...  
Keyword(s):  
Facial Nerve ◽  
Nerve Regeneration ◽  
Dental Pulp ◽  
Dental Pulp Cells ◽  
Nerve Conduits ◽  
Pulp Cells

Luminal Fillers in Nerve Conduits for Peripheral Nerve Repair

2006 ◽  
Vol 57 (4) ◽  
pp. 462-471 ◽  
Author(s):  
Michael B. Chen ◽  
Feng Zhang ◽  
William C. Lineaweaver
Keyword(s):  
Peripheral Nerve ◽  
Nerve Repair ◽  
Peripheral Nerve Repair ◽  
Nerve Conduits

Abstract 3863: Deletion Of Integrin Alpha7 Leads To Altered Cardiac Conduction And Sudden Death Associated With Connexin43 Downregulation

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Raja Nadif ◽  
Michael Emerson ◽  
Ulrike Mayer ◽  
Ludwig Neyses ◽  
Elizabeth Cartwright
Keyword(s):  
Atrial Fibrillation ◽  
Extracellular Matrix ◽  
Ventricular Hypertrophy ◽  
Structural Changes ◽  
Cellular Adhesion ◽  
Left Ventricular ◽  
Cardiac Conduction ◽  
Cardiac Phenotype ◽  
One Year ◽  
Deficient Mice

Effective propagation of the electrical impulse throughout the myocardium is highly dependent on cell-to-cell and cell-to-extracellular matrix interactions. Increasing evidence indicates that dysregulation of cellular adhesion is a critical determinant in the genesis of arrhythmia. Null mutations in the integrin α7 gene, an essential mediator of cellular adhesion in cardiac and skeletal muscles, have been linked to myopathy in humans, however, the in vivo role of the integrin α7 subunit in the heart is undefined. The mouse model of integrin α7 deletion dies prematurely at one year of age. We therefore analysed the cardiac phenotype in integrin α7 deficient mice (α7 −/− ) to determine whether their premature death was associated with altered cardiac conduction. One year old integrin α7 −/− mice exhibited altered cardiac conduction characterised by spontaneous atrial fibrillation and prolonged QTc duration (α7 −/− : 25.7±0.74ms, α7 +/+ : 19.5±0.61ms; n=6; p<0.001, QTc=QT/(RR/100) 1/2 ). The abnormal cardiac conduction was associated with downregulation of connexin43. However, no significant changes were observed in the expression of ion chanels that have been linked to long QT syndrome or atrial fibrillation (kv1.1, kv1.5, kcne1, kcnq1, erg1, Cav1.2 and Cav1.3). In addition, α7 −/− mice displayed increased susceptibility to drug-induced arrhythmias: treatment with ouabain (2mg/kg BW) in combination with isoprenaline (2.5mg/kg BW) induced atrial fibrillation and ventricular tachycardia and eventually death in 6 month-old integrin α7 −/− mice, but not in α7 +/+ mice. Interestingly, α7 −/− also displayed concentric ventricular hypertrophy with increased septal wall thickness and reduced left ventricular end-diastolic diameter starting from 6 months of age. These structural changes were accompanied by an increase in myocyte size and increased ERK1/2 phosphorylation. In conclusion, deletion of the integrin α7 gene in mice leads to ventricular hypertrophy and to abnormal cardiac conduction. The integrin α7 deficient mice have a marked propensity to lethal arrhythmias through alterations in gap junctions but not ion channels. The integrin α7 knockout model provides new insight into the link between the extracellular matrix and cardiac conduction.

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