Abstract
Corneal transplantation remains the ultimate treatment option for advanced stromal and endothelial disorders. Corneal tissue engineering has gained increasing interest in recent years, as it can bypass many complications of conventional corneal transplantation. The human cornea is an ideal organ for tissue engineering, as it is avascular and immune-privileged. Mimicking the complex mechanical properties, the surface curvature, and stromal cytoarchitecure of the in vivo corneal tissue remains a great challenge for tissue engineering approaches. For this reason, automated biofabrication strategies, such as bioprinting, may offer additional spatial control during the manufacturing process to generate full-thickness cell-laden 3D corneal constructs. In this review, we discuss recent advances in bioprinting and biomaterials used for in vitro and ex vivo corneal tissue engineering, corneal cell-biomaterial interactions after bioprinting, and future directions of corneal bioprinting aiming at engineering a full-thickness human cornea in the lab.
Highlights
The human cornea, approximately 550 μm thick in the center and 650 μm in the periphery, is a transparent, dome-shaped tissue covering the front of the eye (Figure 1A) [1]
Corneal clarity is due to the keratocytes that biosynthesize crystallins and organize regularly arranged collagen lamellae, relative avascularity as well as corneal dehydration that is regulated by corneal endothelial cells (Figure 1) [1]
Limbal stem cells (LSCs) that reside in the palisades of Vogt of the peripheral cornea (Figure 2C, white circles) continuously regenerate corneal epithelial cells (CEpCs)
Summary
The human cornea, approximately 550 μm thick in the center and 650 μm in the periphery, is a transparent, dome-shaped tissue covering the front of the eye (Figure 1A) [1]. Corneal stromal keratocytes are flattened dendritic cells, 31 μm wide and about 1 μm thick, predominantly disposed in the interface between adjacent lamellae They produce and reorganize the ECM, secrete collagen and proteoglycans (keratan sulfate proteoglycan (KSPG); lumican, keratocan, and mimecan) which can influence the fibril spacing and optimize the optical characteristics of the cornea [1,4]. Infection or injury can wound the stroma which causes CSKs at the injured site to die, while the surviving CSKs at the wound periphery are “activated” to assume a repair cell type, the stromal fibroblasts (SFs) They are proliferative and motile cells with an attenuated expression of CSK genes and proteins (including keratocan, aldehyde dehydrogenase (ALDH), transketolase) but display a fibrosis-related gene profile (including fibronectin, tenascin, SPACR, and metalloproteinases) [4]. Corneal endothelial disorders currently represent the most common reason for corneal transplantation in industrialized countries [13]
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