While electrospinning had seen intermittent use in the textile industry from the early twentieth century, it took the explosion of the field of tissue engineering, and its pursuit of biomimetic extracellular matrix (ECM) structures, to create an electrospinning renaissance. Over the past decade, a growing number of researchers in the tissue engineering community have embraced electrospinning as a polymer processing technique that effectively and routinely produces non‐woven structures of nanoscale fibers (sizes of 80 nm to 1.5 µm). These nanofibers are of physiological significance as they closely resemble the structure and size scale of the native ECM (fiber diameters of 50 to 500 nm). Attempts to replicate the many roles of native ECM have led to the electrospinning of a wide array of polymers, both synthetic (poly(glycolic acid), poly(lactic acid), polydioxanone, polycaprolactone, etc.) and natural (collagen, fibrinogen, elastin, etc.) in origin, for a multitude of different tissue applications. With various compositions, fiber dimensions and fiber orientations, the biological, chemical and mechanical properties of the electrospun materials can be tailored. In this review we highlight the role of electrospinning in the engineering of different tissues and applications (skin/wound healing, cartilage, bone, vascular tissue, urological tissues, nerve, and ligament), and discuss its potential role in future work. Copyright © 2007 Society of Chemical Industry
Fibrinogen has a well-established tissue engineering track record because of its ability to induce improved cellular interaction and scaffold remodeling compared to synthetic scaffolds. While the feasibility of electrospinning fibrinogen scaffolds of submicron diameter fibers and their mechanical properties have been demonstrated, in vitro cellular interaction has not yet been evaluated. The goal of this study was to demonstrate, based on cellular interaction and scaffold remodeling, that electrospun fibrinogen can be used successfully as a tissue engineering scaffold. Electrospun fibrinogen scaffolds were disinfected, seeded with neonatal rat cardiac fibroblasts, and cultured for 2, 7, and 14 days. Cultures were treated to regulate scaffold degradation by either supplementing serum-containing media with aprotinin or crosslinking the scaffolds with glutaraldehyde vapor. Biocompatibility was assessed through a WST-1 cell proliferation assay. Postculture scaffolds were evaluated by scanning electron microscopy and histology. Cell culture demonstrated that fibroblasts readily migrate into and remodel electrospun fibrinogen scaffolds with deposition of native collagen. Supplementation of culture media with different concentrations of aprotinin-modulated scaffold degradation in a predictable fashion, but glutaraldehyde vapor fixation was less reliable. Based on the observed cellular interactions, there is tremendous potential for electrospun fibrinogen as a tissue engineering scaffold.
The purpose of this study was to demonstrate that human bladder smooth muscle cells (HBSM) remodel electrospun fibrinogen mats. Fibrinogen scaffolds were electrospun and disinfected using standard methods. Scaffolds were seeded with 5 x 10(4) HBSM per scaffold. Cultures were supplemented with aprotinin concentrations of 0 KIU ml(-1) (no aprotinin), 100 KIU ml(-1) or 1000 KIU ml(-1) and incubated with twice weekly media changes. Samples were removed for evaluation at 1, 3, 7 and 14 days. Cultured scaffolds were evaluated with a WST-1 cell proliferation assay, scanning electron microscopy and histology. Cell culture demonstrated that HBSM readily migrated into and initiated remodelling of the electrospun fibrinogen scaffolds by deposition of collagen. Proliferation was suppressed during this initial phase with respect to a 2D control due to cell migration. Histology confirmed that proliferation increased during the later stages of remodelling. Remodelling was slower at higher aprotinin concentrations. These results demonstrate that HBSM rapidly remodel an electrospun fibrinogen scaffold and deposit native collagen. The process can be modulated using aprotinin, a protease inhibitor. These initial findings indicate that there is tremendous potential for electrospun fibrinogen as a urologic tissue engineering scaffold with the ultimate goal of producing an implantable acellular product that would promote cellular in-growth and in situ tissue regeneration.
Our objective is to demonstrate an electrospun fibrinogen-PDO (polydioxanone) composite scaffold will retain the superior cellular interaction of fibrinogen while producing a product with the functional strength needed for direct implantation. Fibrinogen-PDO composite scaffolds were electrospun with PDO ratios of 0% (pure fibrinogen), 10%, 20%, 30%, 40%, 50% and 100% (pure PDO) and disinfected using standard methods. Scaffolds were seeded with human BSM (bladder smooth muscle cells) and incubated with twice weekly media changes. Samples were removed at 7, 14 and 21 days for evaluation by collagen assay, scanning electron microscopy and histology. Cell seeding and culture demonstrated human BSM readily migrate throughout and remodel electrospun fibrinogen-PDO composite scaffolds with deposition of native collagen. Cell migration and collagen deposition increased with increasing fibrinogen concentration while scaffold integrity increased with increasing PDO concentration. Electrospun fibrinogen-PDO composite structures promote rapid cellular in-growth by human BSM while maintaining structural integrity. The fibrinogen to PDO ratio can be adjusted to achieve the desired properties required for a specific tissue engineering application. Our ultimate objective is to utilize this innovative biomaterial technology to produce an acellular, bioresorbable product that enables in situ tissue regeneration. While there is still much work to be done, these initial findings indicate fibrinogen-PDO composite scaffolds deserve further investigation.
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