A multilayered scaffold for regeneration of smooth muscle and connective tissue layers.

Tissue regeneration often requires recruitment of different cell types and rebuilding of two or more tissue layers to restore function. Here, we describe the creation of a novel multilayered scaffold with distinct fiber organizations-aligned to unaligned and dense to porous-to template common architectures found in adjacent tissue layers. Electrospun scaffolds were fabricated using a biodegradable, tyrosine-derived terpolymer, yielding densely-packed, aligned fibers that transition into randomly-oriented fibers of increasing diameter and porosity.

A step toward engineering thick tissues: Distributing microfibers within 3D printed frames.

Microfiber mats for tissue engineering scaffolds support cell growth, but are limited by poor cell infiltration and nutrient transport. Three-dimensional printing, specifically fused deposition modeling (FDM), can rapidly produce customized constructs, but macroscopic porosity resulting from low resolution reduces cell seeding efficiency and prevents the formation of continuous cell networks. Here we describe the fabrication of hierarchical scaffolds that integrate a fibrous microenvironment with the open macropore structure of FDM.

Development of hybrid scaffolds with natural extracellular matrix deposited within synthetic polymeric fibers.

A major challenge of tissue engineering is to generate materials that combine bioactivity with stability in a form that captures the robust nature of native tissues. Here we describe a procedure to fabricate a novel hybrid extracellular matrix (ECM)-synthetic scaffold biomaterial by cell-mediated deposition of ECM within an electrospun fiber mat. Synthetic polymer fiber mats were fabricated using poly(desamino tyrosyl-tyrosine carbonate) (PDTEC) co-spun with poly(ethylene glycol) (PEG) used as a sacrificial polymer.

Stimulatory effects of advanced glycation endproducts (AGEs) on fibronectin matrix assembly.

Advanced glycation endproducts (AGEs) are a heterogeneous group of compounds that form via non-enzymatic glycation of proteins throughout our lifespan and at a higher rate in certain chronic diseases such as diabetes. AGEs contribute to the progression of fibrosis, in part by stimulating cellular pathways that affect gene expression. Long-lived ECM proteins are targets for non-enzymatic glycation but the question of whether the AGE-modified ECM leads to excess ECM accumulation and fibrosis remains unanswered.