scholarly journals N-Isopropylacrylamide-co-glycidylmethacrylate as a Thermoresponsive Substrate for Corneal Endothelial Cell Sheet Engineering

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Bernadette K. Madathil ◽  
Pallickaveedu RajanAsari Anil Kumar ◽  
Thrikkovil Variyath Kumary
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cell ◽  
Cell Sheet ◽  
Corneal Endothelial Cell ◽  
Solution Temperature ◽  
Pcr Analysis ◽  
Cell Contact ◽  
Endothelial Keratoplasty ◽  
Matrix Deposition ◽  
Stimuli Responsive Polymers

Endothelial keratoplasty is a recent shift in the surgical treatment of corneal endothelial dystrophies, where the dysfunctional endothelium is replaced whilst retaining the unaffected corneal layers. To overcome the limitation of donor corneal shortage, alternative use of tissue engineered constructs is being researched. Tissue constructs with intact extracellular matrix are generated using stimuli responsive polymers. In this study we evaluated the feasibility of using the thermoresponsive poly(N-isopropylacrylamide-co-glycidylmethacrylate) polymer as a culture surface to harvest viable corneal endothelial cell sheets. Incubation below the lower critical solution temperature of the polymer allowed the detachment of the intact endothelial cell sheet. Phase contrast and scanning electron microscopy revealed the intact architecture, cobble stone morphology, and cell-to-cell contact in the retrieved cell sheet. Strong extracellular matrix deposition was also observed. The RT-PCR analysis confirmed functionally active endothelial cells in the cell sheet as evidenced by the positive expression of aquaporin 1, collagen IV, Na+-K+ATPase, and FLK-1. Na+-K+ATPase protein expression was also visualized by immunofluorescence staining. These results suggest that the in-house developed thermoresponsive culture dish is a suitable substrate for the generation of intact corneal endothelial cell sheet towards transplantation for endothelial keratoplasty.

scholarly journals Corneal endothelial cell dysfunction: etiologies and management

2018 ◽  
Vol 10 ◽  
pp. 251584141881580 ◽  
Author(s):  
Sepehr Feizi
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Endothelial Dysfunction ◽  
Corneal Endothelial Cell ◽  
Endothelial Cell Dysfunction ◽  
Endothelial Keratoplasty ◽  
Corneal Endothelial Cells ◽  
Cell Dysfunction ◽  
Corneal Endothelial Dysfunction

A transparent cornea is essential for the formation of a clear image on the retina. The human cornea is arranged into well-organized layers, and each layer plays a significant role in maintaining the transparency and viability of the tissue. The endothelium has both barrier and pump functions, which are important for the maintenance of corneal clarity. Many etiologies, including Fuchs’ endothelial corneal dystrophy, surgical trauma, and congenital hereditary endothelial dystrophy, lead to endothelial cell dysfunction. The main treatment for corneal decompensation is replacement of the abnormal corneal layers with normal donor tissue. Nowadays, the trend is to perform selective endothelial keratoplasty, including Descemet stripping automated endothelial keratoplasty and Descemet’s membrane endothelial keratoplasty, to manage corneal endothelial dysfunction. This selective approach has several advantages over penetrating keratoplasty, including rapid recovery of visual acuity, less likelihood of graft rejection, and better patient satisfaction. However, the global limitation in the supply of donor corneas is becoming an increasing challenge, necessitating alternatives to reduce this demand. Consequently, in vitro expansion of human corneal endothelial cells is evolving as a sustainable choice. This method is intended to prepare corneal endothelial cells in vitro that can be transferred to the eye. Herein, we describe the etiologies and manifestations of human corneal endothelial cell dysfunction. We also summarize the available options for as well as recent developments in the management of corneal endothelial dysfunction.

scholarly journals EphB2 and EphB4 receptors forward signaling promotes SDF-1–induced endothelial cell chemotaxis and branching remodeling

Blood ◽  
2006 ◽  
Vol 108 (9) ◽  
pp. 2914-2922 ◽  
Author(s):  
Ombretta Salvucci ◽  
Maria de la Luz Sierra ◽  
Jose A. Martina ◽  
Peter J. McCormick ◽  
Giovanna Tosato
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cell ◽  
Tyrosine Kinases ◽  
Molecular Mechanisms ◽  
Cell Movement ◽  
Cell Contact ◽  
Eph Receptor ◽  
Cell Clustering ◽  
Chemokine Ligand ◽  
Ephrin Ligands

Abstract The complex molecular mechanisms that drive endothelial cell movement and the formation of new vessels are poorly understood and require further investigation. Eph receptor tyrosine kinases and their membrane-anchored ephrin ligands regulate cell movements mostly by cell–cell contact, whereas the G-protein–coupled receptor CXCR4 and its unique SDF-1 chemokine ligand regulate cell movement mostly through soluble gradients. By using biochemical and functional approaches, we investigated how ephrinB and SDF-1 orchestrate endothelial cell movement and morphogenesis into capillary-like structures. We describe how endogenous EphB2 and EphB4 signaling are required for the formation of extracellular matrix–dependent capillary-like structures in primary human endothelial cells. We further demonstrate that EphB2 and EphB4 activation enhance SDF-1–induced signaling and chemotaxis that are also required for extracellular matrix–dependent endothelial cell clustering. These results support a model in which SDF-1 gradients first promote endothelial cell clustering and then EphB2 and EphB4 critically contribute to subsequent cell movement and alignment into cord-like structures. This study reveals a requirement for endogenous Eph signaling in endothelial cell morphogenic processes, uncovers a novel link between EphB forward signaling and SDF-1–induced signaling, and demonstrates a mechanism for cooperative regulation of endothelial cell movement.

Cultivated Corneal Endothelial Cell Sheet Transplantation in a Primate Model

2007 ◽  
Vol 48 (10) ◽  
pp. 4519 ◽  
Author(s):  
Noriko Koizumi ◽  
Yuji Sakamoto ◽  
Naoki Okumura ◽  
Norio Okahara ◽  
Hideaki Tsuchiya ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Sheet ◽  
Corneal Endothelial Cell ◽  
Primate Model

scholarly journals Association between aqueous humor cytokines and postoperative corneal endothelial cell loss after Descemet stripping automated endothelial keratoplasty

PLoS ONE ◽  
2021 ◽  
Vol 16 (12) ◽  
pp. e0260963
Author(s):  
Tatsu Okabe ◽  
Wataru Kobayashi ◽  
Takehiro Hariya ◽  
Shunji Yokokura ◽  
Toru Nakazawa
Keyword(s):  
Endothelial Cell ◽  
Aqueous Humor ◽  
Rank Correlation ◽  
Cell Loss ◽  
Corneal Endothelial Cell ◽  
University Hospital ◽  
Endothelial Keratoplasty ◽  
Spearman’S Rank Correlation ◽  
Spearman’S Rank Correlation Coefficient ◽  
Multiplex Bead

This study measured the intraoperative anterior aqueous humor concentrations of various cytokines during corneal endothelial transplantation and searched for relationships between these concentrations and postoperative corneal endothelial cell (CEC) depletion. We recruited 30 consecutive patients who underwent corneal endothelial transplantation with Descemet’s stripping automated endothelial keratoplasty (DSAEK) at Tohoku University Hospital between February 2014 and July 2017. During surgery, we obtained aqueous humor samples and later measured the concentrations of 27 cytokines with a Multiplex Bead Assay (Bio-Plex Pro). We counted CECs 1, 6 and 12 months after surgery, and used Spearman’s rank correlation coefficient to identify relationships between CEC depletion and the concentrations of detected cytokines. The loss of CECs 1–6 months after surgery was significantly correlated with IL-7, IP-10, MIP-1a and MIP-1b concentrations (-0.67, -0.48, -0.39, and -0.45, respectively, all P <0.01). CEC loss 1–12 months after surgery was significantly correlated with IL-1b, IL-7, IP-10 and RANTES concentrations (-0.46, -0.52, -0.48, and -0.43, respectively). Multiple regression analysis showed that IL-7 concentration was significantly associated with CEC loss 1–6 months after surgery (b = -0.65, P < 0.01) and IP-10 concentration was associated with CEC loss 1–12 months after surgery (β = -0.38, P < 0.05). These results suggest that not only inflammatory cytokines but also IL-7, a cytokine related to lymphocytes, may be involved in the depletion of CECs after DSAEK, particularly depletion that occurs relatively early.

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