scholarly journals Reconstituted epithelial tissues and native cornea: A comparison of the influence of surfactants on ocular permeability

Author(s):  
Erica Zucchetti ◽  
Daniela Monti ◽  
Patrizia Chetoni ◽  
Silvia Tampucci ◽  
Susi Burgalassi

The aim of this study was to prepare an artificial rabbit corneal epithelium (RRCE) to compare with a human corneal epithelial model and excised rabbit cornea through permeation studies to investigate differences of surfactants influence on ocular permeability of a lipophilic compound. First solubility assays with different surfactants were performed and the integrity of the RRCE was assessed by measuring transepithelial electrical resistance (TEER). The permeation parameters showed that the RRCE was more sensitive than native cornea and human cornal epithelial model to the effect of permeation enhancers.

2004 ◽  
Vol 20 (6) ◽  
pp. 518-532 ◽  
Author(s):  
Susi Burgalassi ◽  
Daniela Monti ◽  
Annalisa Brignoccoli ◽  
Ortenzio Fabiani ◽  
Carla Lenzi ◽  
...  

Lab on a Chip ◽  
2021 ◽  
Author(s):  
A. Nicolas ◽  
F. Schavemaker ◽  
K. Kosim ◽  
D. Kurek ◽  
M. Haarmans ◽  
...  

We present an instrument for simultaneously measuring TEER in up to 80 perfused epithelial tubules on an OrganoPlate. The sensitivity, speed and ease of use enables screening of tubules during formation, drug exposure and inflammatory processes.


1998 ◽  
Vol 17 (1) ◽  
pp. 47-52 ◽  
Author(s):  
Shizuya Saika ◽  
Yoshiji Kawashima ◽  
Yuka Okada ◽  
Sai-Ichi Tanaka ◽  
Osamu Yamanaka ◽  
...  

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Mingsen Li ◽  
Liqiong Zhu ◽  
Jiafeng Liu ◽  
Huaxing Huang ◽  
Huizhen Guo ◽  
...  

AbstractForkhead box C1 (FOXC1) is required for neural crest and ocular development, and mutations in FOXC1 lead to inherited Axenfeld–Rieger syndrome. Here, we find that FOXC1 and paired box 6 (PAX6) are co-expressed in the human limbus and central corneal epithelium. Deficiency of FOXC1 and alternation in epithelial features occur in patients with corneal ulcers. FOXC1 governs the fate of the corneal epithelium by directly binding to lineage-specific open promoters or enhancers marked by H3K4me2. FOXC1 depletion not only activates the keratinization pathway and reprograms corneal epithelial cells into skin-like epithelial cells, but also disrupts the collagen metabolic process and interferon signaling pathways. Loss of interferon regulatory factor 1 and PAX6 induced by FOXC1 dysfunction is linked to the corneal ulcer. Collectively, our results reveal a FOXC1-mediated regulatory network responsible for corneal epithelial homeostasis and provide a potential therapeutic target for corneal ulcer.


Antioxidants ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 128
Author(s):  
Grazia Maugeri ◽  
Agata Grazia D’Amico ◽  
Salvatore Giunta ◽  
Cesarina Giallongo ◽  
Daniele Tibullo ◽  
...  

The corneal epithelium, the outermost layer of the cornea, acts as a dynamic barrier preventing access to harmful agents into the intraocular space. It is subjected daily to different insults, and ultraviolet B (UV-B) irradiation represents one of the main causes of injury. In our previous study, we demonstrated the beneficial effects of pituitary adenylate cyclase-activating polypeptide (PACAP) against UV-B radiation damage in the human corneal endothelium. Some of its effects are mediated through the activation of the intracellular factor, known as the activity-dependent protein (ADNP). In the present paper, we have investigated the role of ADNP and the small peptide derived from ADNP, known as NAP, in the corneal epithelium. Here, we have demonstrated, for the first time, ADNP expression in human and rabbit corneal epithelium as well as its protective effect by treating the corneal epithelial cells exposed to UV-B radiations with NAP. Our results showed that NAP treatment prevents ROS formation by reducing UV-B-irradiation-induced apoptotic cell death and JNK signalling pathway activation. Further investigations are needed to deeply investigate the possible therapeutic use of NAP to counteract corneal UV-B damage.


2000 ◽  
Vol 11 (3) ◽  
pp. 413-422
Author(s):  
JOSÉ G. VAN DEN BERG ◽  
JAN ATEN ◽  
M. ANWAR CHAND ◽  
NIKE CLAESSEN ◽  
LISETTE DIJKINK ◽  
...  

Abstract. In minimal change nephrosis (MCN), proteinuria is associated with structural changes of the glomerular visceral epithelial cells (GVEC). The occurrence of MCN has been associated with T-helper2 lymphocyte-dependent conditions. To examine a direct role for type 2 cytokines in GVEC injury, the expression of interleukin (IL)-4/IL-13 receptors by GVEC and direct effects of IL-4 and IL-13 on GVEC were studied. Reverse transcription-PCR showed that isolated human and rat glomeruli and cultured human and rat GVEC expressed mRNA for IL-4Rα, IL-13Rα1, and IL-13Rα2. Protein expression of IL-4Rα and IL-13Rα2 by GVEC in human kidney biopsies and by cultured human GVEC was detected by immunohistochemistry. Western blotting demonstrated phosphorylation of STAT6 in cultured GVEC upon incubation with IL-4 or IL-13. This indicated signal transduction via the heterodimeric receptor complex IL-4R2, which is composed of the IL-4Rα and the IL-13Rα1. Direct effects on GVEC function were examined in monolayer experiments. IL-4 and IL-13 dose-dependently decreased transepithelial electrical resistance of monolayers of rat GVEC to approximately 30 and 40% of baseline values, respectively. The transepithelial electrical resistance decrease was associated with a significant increase in short-circuit current, whereas no changes were observed in the transmonolayer flux of the macromolecules horseradish peroxidase (molecular weight, 44 kD) and 14C-mannitol (molecular weight, 182 Da). No changes in cell structure were observed with electron microscopy. It is concluded that by binding to specific IL-4/IL-13 receptors, IL-4 and IL-13 can exert specific effects on GVEC function, which could be of pathogenetic relevance for glomerular injury in MCN.


2014 ◽  
Vol 39 (7) ◽  
pp. 686-694 ◽  
Author(s):  
Kinya Iwatsuka ◽  
Hiroki Iwamoto ◽  
Mitsuhiro Kinoshita ◽  
Katsuhiro Inada ◽  
Shin-ichi Yasueda ◽  
...  

2016 ◽  
Vol 3 (10) ◽  
pp. 160658 ◽  
Author(s):  
Amy S. Findlay ◽  
D. Alessio Panzica ◽  
Petr Walczysko ◽  
Amy B. Holt ◽  
Deborah J. Henderson ◽  
...  

This study shows that the core planar cell polarity (PCP) genes direct the aligned cell migration in the adult corneal epithelium, a stratified squamous epithelium on the outer surface of the vertebrate eye. Expression of multiple core PCP genes was demonstrated in the adult corneal epithelium. PCP components were manipulated genetically and pharmacologically in human and mouse corneal epithelial cells in vivo and in vitro . Knockdown of VANGL2 reduced the directional component of migration of human corneal epithelial (HCE) cells without affecting speed. It was shown that signalling through PCP mediators, dishevelled, dishevelled-associated activator of morphogenesis and Rho-associated protein kinase directs the alignment of HCE cells by affecting cytoskeletal reorganization. Cells in which VANGL2 was disrupted tended to misalign on grooved surfaces and migrate across, rather than parallel to the grooves. Adult corneal epithelial cells in which Vangl2 had been conditionally deleted showed a reduced rate of wound-healing migration. Conditional deletion of Vangl2 in the mouse corneal epithelium ablated the normal highly stereotyped patterns of centripetal cell migration in vivo from the periphery (limbus) to the centre of the cornea. Corneal opacity owing to chronic wounding is a major cause of degenerative blindness across the world, and this study shows that Vangl2 activity is required for directional corneal epithelial migration.


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