Cell–Matrix Interactions in the Eye: From Cornea to Choroid

Abstract

The extracellular matrix (ECM) plays a crucial role in all parts of the eye, from maintaining clarity and hydration of the cornea and vitreous to regulating angiogenesis, intraocular pressure maintenance, and vascular signaling. This review focuses on the interactions of the ECM for homeostasis of normal physiologic functions of the cornea, vitreous, retina, retinal pigment epithelium, Bruch’s membrane, and choroid as well as trabecular meshwork, optic nerve, conjunctiva and tenon’s layer as it relates to glaucoma. A variety of pathways and key factors related to ECM in the eye are discussed, including but not limited to those related to transforming growth factor-β, vascular endothelial growth factor, basic-fibroblastic growth factor, connective tissue growth factor, matrix metalloproteinases (including MMP-2 and MMP-9, and MMP-14), collagen IV, fibronectin, elastin, canonical signaling, integrins, and endothelial morphogenesis consistent of cellular activation-tubulogenesis and cellular differentiation-stabilization. Alterations contributing to disease states such as wound healing, diabetes-related complications, Fuchs endothelial corneal dystrophy, angiogenesis, fibrosis, age-related macular degeneration, retinal detachment, and posteriorly inserted vitreous base are also reviewed.

MicroRNAs Expression in Response to rhNGF in Epithelial Corneal Cells: Focus on Neurotrophin Signaling Pathway

“…DIANA-TarBase and microT-CDS algorithms (genes union function) were used to identify experimentally supported and predicted miRNA/target-mRNA interactions, respectively, as well as significant KEGG pathways, in which target genes were involved ( Table 2 and Table 3 ). Among them emerged the ECM-receptor interaction and the focal adhesion pathways, already described in cornea homeostasis and normal physiological functions [ 27 ], corneal epithelial cell motility [ 28 ], neovascularization [ 29 ] and adhesion [ 30 , 31 ], the Hippo signaling pathway, playing a role in limbal cell proliferation, corneal wound healing and regeneration [ 32 , 33 ] and, as expected, the Neurotrophin signaling pathway. The latter was considered for more in-depth analysis: sixty and fifty genes, targeted by 18 and 16 out of 21 miRNAs (miR-337-5p, mir-34a-3p, mir-1227-3p did not show any target gene) were detected by DIANA-TarBase and microT-based analysis, respectively ( Table 4 ).…”

Autophagy in Extracellular Matrix and Wound Healing Modulation in the Cornea

“…Matrix metalloproteinases (MMPs) are enzymes implicated in the degradation/destruction of ECM components and basement membrane, angiogenesis, and wound healing. MMP-14 is an important MMP associated with angiogenesis and ECM remodeling in the corneal homeostasis [ 27 ]. A previous study showed that corneal injury-associated mast cell activation significantly increased the levels of CCL2 and TNF-α and neutrophil recruitment [ 92 ].…”

“…Corneal transparency is maintained by the precise organization and orientation of the collagen fibrils of the ECM. Altered ECM deposition/degradation changes normal corneal function and induces corneal disease pathologies, including scarring that affects corneal transparency [ 25 , 26 , 27 ].…”

Age-Related Macular Degeneration Masquerade: A Review of Pentosan Polysulfate Maculopathy and Implications for Clinical Practice

“…Given the similarity of PPS maculopathy to mitochondrial maculopathies, Yusuf et al 38 proposed that PPS altered mitochondrial function through an unknown mechanism. Hanif and coworkers proposed 2 other possibilities based on the similarity of the structure of the composite glycosaminoglycans to PPS itself: direct toxicity to RPE that would inhibit processing of photoreceptor outer segments or disruption of the interphotoreceptor matrix that mediates the photoreceptor-RPE relationship, especially because the insoluble components of the interphotoreceptor matrix are comprised of chondroitin sulfate proteoglycans 33,39 . Findings of choriocapillaris dropout may implicate a vascular cause as is the case in early and late AMD 40–42 …”