scholarly journals Utilização do flap de Gundersen para tratamento de disfunção endotelial em equino – relato de caso

2021 ◽  
Vol 4 (5) ◽  
pp. 32-38
Author(s):  
Cleydianne Rodrigues de Almeida ◽  
◽  
Cleyber José da Trindade de Fátima ◽  
Rômulo Vitelli Rocha Peixoto ◽  
Anderson Farias ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Corneal Ulcer ◽  
Corneal Edema ◽  
Corneal Endothelial Cells ◽  
Eye Care ◽  
Visual Axis ◽  
Lens Dislocation ◽  
Uveitis Anterior ◽  
Ulcerative Keratitis

Endothelial dysfunction in horses is associated with dystrophy or degeneration of corneal endothelial cells, clinically presented as a diffuse corneal edema unresponsive to conventional treatments. The main causes of such injury are trauma, ulcerative keratitis, recurrent uveitis, anterior lens dislocation and glaucoma. This paper aims to report a case of endothelial dysfunction in a mare, diagnosed with endothelial dysfunction after uveitis, glaucoma and indolent corneal ulcer. For correction, a superficial lamellar keratectomy followed by permanent conjunctival graft, described as a Gundersen flap, was performed. After intensive eye care, he returned to his athletic functions, maintained corneal and visual axis transparency and ocular reflexes.

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 MitoROS due to loss of Slc4a11 in corneal endothelial cells induces ER stress, lysosomal dysfunction and impairs autophagy

2020 ◽  
Author(s):  
Rajalekshmy Shyam ◽  
Diego G. Ogando ◽  
Moonjung Choi ◽  
Joseph A. Bonanno
Keyword(s):  
Endothelial Cells ◽  
Er Stress ◽  
Corneal Edema ◽  
Corneal Endothelial Cells ◽  
Autophagy Flux ◽  
Unfolded Protein ◽  
Stress Markers ◽  
Lysosomal Dysfunction ◽  
Mitochondrial Ros ◽  
Elevated Expression

AbstractRecent studies from Slc4a11 KO mice have identified mitochondrial dysfunction as a major contributor toward oxidative stress and cell death in Congenital Hereditary Endothelial Dystrophy. Here we asked if this stress activated autophagy in the Slc4a11 KO cell line and in KO mouse endothelial tissue. Early indicators of autophagy, phospho-mTOR and LC3-II indicated activation, however P62 was elevated suggesting an impairment of autophagy flux. The activity and the number of lysosomes, the organelle responsible for the final degradation of autophagy substrates, were found to be reduced in the KO. In addition, the expression of the master regulator of lysosomal function and biogenesis, TFEB, was significantly reduced in the KO corneal endothelia. Also, we observed increased Unfolded Protein Response, as well as elevated expression of ER stress markers, BIP and CHOP. To test if lysosomal and ER stress stems from elevated mitochondrial ROS, we treated Slc4a11 KO corneal endothelial cells with the mitochondrial ROS quencher, MitoQ. MitoQ restored lysosomal enzymes as well as TFEB, reduced ER stress, and increased autophagy flux. MitoQ injections of Slc4a11 KO mice decreased corneal edema, the major phenotype associated with CHED. We conclude that mitochondrial ROS causes ER stress and lysosomal dysfunction with impairment of autophagy in Slc4a11 KO corneal endothelium. Our study is the first to identify the presence as well as cause of lysosomal dysfunction and ER stress in an animal model of CHED, and to characterize inter-organelle relationship in a corneal cell type.

scholarly journals NAD+ precursors protect corneal endothelial cells from UVB-induced apoptosis

2020 ◽  
Vol 318 (4) ◽  
pp. C796-C805 ◽  
Author(s):  
Can Zhao ◽  
Wenjing Li ◽  
Haoyun Duan ◽  
Zongyi Li ◽  
Yanni Jia ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Apoptosis ◽  
Corneal Endothelium ◽  
Corneal Edema ◽  
Ultraviolet B ◽  
Subconjunctival Injection ◽  
Corneal Endothelial Cells ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Mesenchymal Transition ◽  
Induced Apoptosis

Excessive exposure of the eye to ultraviolet B light (UVB) leads to corneal edema and opacification because of the apoptosis of the corneal endothelium. Our previous study found that nicotinamide (NIC), the precursor of nicotinamide adenine dinucleotide (NAD), could inhibit the endothelial-mesenchymal transition and accelerate healing the wound to the corneal endothelium in the rabbit. Here we hypothesize that NIC may possess the capacity to protect the cornea from UVB-induced endothelial apoptosis. Therefore, a mouse model and a cultured cell model were used to examine the effect of NAD+ precursors, including NIC, nicotinamide mononucleotide (NMN), and NAD, on the UVB-induced apoptosis of corneal endothelial cells (CECs). The results showed that UVB irradiation caused apparent corneal edema and cell apoptosis in mice, accompanied by reduced levels of NAD+ and its key biosynthesis enzyme, nicotinamide phosphoribosyltransferase (NAMPT), in the corneal endothelium. However, the subconjunctival injection of NIC, NMN, or NAD+ effectively prevented UVB-induced tissue damage and endothelial cell apoptosis in the mouse cornea. Moreover, pretreatment using NIC, NMN, and NAD+ increased the survival rate and inhibited the apoptosis of cultured human CECs irradiated by UVB. Mechanistically, pretreatment using nicotinamide (NIC) recovered the AKT activation level and decreased the BAX/BCL-2 ratio. In addition, the capacity of NIC to protect CECs was fully reversed in the presence of the AKT inhibitor LY294002. Therefore, we conclude that NAD+ precursors can effectively prevent the apoptosis of the corneal endothelium through reactivating AKT signaling; this represents a potential therapeutic approach for preventing UVB-induced corneal damage.

scholarly journals Persimmon Leaves (Diospyros kaki) Extract Enhances the Viability of Human Corneal Endothelial Cells by Improving Na+-K+-ATPase Activity

2022 ◽  
Vol 15 (1) ◽  
pp. 72
Author(s):  
Ramsha Afzal ◽  
Hyung Bin Hwang
Keyword(s):  
Endothelial Cells ◽  
Atpase Activity ◽  
Basolateral Membrane ◽  
Corneal Edema ◽  
Ethanol Extract ◽  
Diospyros Kaki ◽  
Corneal Endothelial Cells ◽  
Human Corneal Endothelial Cells ◽  
Corneal Decompensation

The Na+/K+-ATPase, present in the basolateral membrane of human corneal endothelial cells (HCECs), is known to play an important role for corneal transparency. Na+/K+-ATPase dysfunction is one of the major causes of corneal decompensation. The ethanol extract of Diospyros kaki (EEDK) has been reported to increase corneal cell viability. Thus, we treated HCECs with EEDK and studied its effects on HCECs survival and Na+/K+-ATPase against cytotoxic drugs like staurosporine (ST) and ouabain (OU). Firstly, survival assays, (MTT assay and live dead-imaging) showed that decreased HCECs viability by ST and OU was significantly recovered by EEDK co-treatment. Secondly, Na+/K+-ATPase activity assays revealed that EEDK enhanced Na+/K+-ATPase enzymatic activity (* p < 0.01) with/without ST and OU. Finally, Na+/K+-ATPase expression analysis (Western Blot and confocal microscopy) demonstrated that EEDK treatment with/without ST and OU facilitates Na+/K+-ATPase expression in HCECs. Taken together, our findings led us to the conclusion that EEDK might aid HCECs survival in vitro by increasing the activity and expression of Na+/K+-ATPase enzyme. Since Na+/K+-ATPase activity is important to maintain cellular function of HCECs, we suggest that EEDK can be a potential effective agent against corneal edema and related corneal disorders.

scholarly journals Long noncoding RNA KCNQ1OT1 induces pyroptosis in diabetic corneal endothelial keratopathy

2020 ◽  
Vol 318 (2) ◽  
pp. C346-C359 ◽  
Author(s):  
Yanyan Zhang ◽  
Zhen Song ◽  
Xuran Li ◽  
Shuo Xu ◽  
Sujun Zhou ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Rna Binding ◽  
Cultured Cells ◽  
Corneal Edema ◽  
Corneal Endothelial Cells ◽  
Caspase 1

Diabetic corneal endothelial keratopathy is an intractable ocular complication characterized by corneal edema and endothelial decompensation, which seriously threaten vision. It has been suggested that diabetes is associated with pyroptosis, a type of programmed cell death via the activation of inflammation. Long noncoding RNA KCNQ1OT1 is commonly associated with various pathophysiological mechanisms of diabetic complications, including diabetic cardiomyopathy and diabetic retinopathy. However, whether KCNQ1OT1 is capable of regulating pyroptosis and participates in the pathogenesis of diabetic corneal endothelial keratopathy remains unknown. The aim of this study was to investigate the mechanisms of KCNQ1OT1 in diabetic corneal endothelial keratopathy. Here, we reveal that KCNQ1OT1 and pyroptosis can be triggered in diabetic human and rat corneal endothelium, along with the high glucose-treated corneal endothelial cells. However, miR-214 expression was substantially decreased in vivo and in experiments with cultured cells. LDH assay was also used to verify the existence of pyroptosis in high glucose-treated cells. Bioinformatics prediction and luciferase assays showed that KCNQ1OT1 may function as a competing endogenous RNA binding miR-214 to regulate the expression of caspase-1. To further analyze the KCNQ1OT1-mediated mechanism, miR-214 mimic and inhibitor were introduced into the high glucose-treated corneal endothelial cells. The results showed that upregulation of miR-214 attenuated pyroptosis; conversely, knockdown of miR-214 promoted it. In addition, KCNQ1OT1 knockdown by a small interfering RNA decreased pyroptosis factors expressions but enhanced miR-214 expression in corneal endothelial cells. To understand the signaling mechanisms underlying the prepyroptotic properties of KCNQ1OT1, si-KCNQ1OT1 was cotransfected with or without miR-214 inhibitor. The results showed that pyroptosis was repressed after silencing KCNQ1OT1 but was reversed by cotransfection with miR-214 inhibitor, suggesting that KCNQ1OT1 mediated pyroptosis induced by high glucose via targeting miR-214. Therefore, the KCNQ1OT1/miR-214/caspase-1 signaling pathway represents a new mechanism of diabetic corneal endothelial keratopathy progression, and KCNQ1OT1 could potentially be a novel therapeutic target.

scholarly journals Early Postoperative Effects of Uncomplicated Phacoemulsification Surgery on Corneal Endothelial Cells and Thickness in Patients with Pseudoexfoliation Syndrome

2021 ◽  
Author(s):  
EREN EKİCİ ◽  
Ali Keles ◽  
Süleyman Korhan Kahraman
Keyword(s):  
Endothelial Cells ◽  
Anterior Chamber ◽  
Coefficient Of Variation ◽  
Corneal Edema ◽  
Pseudoexfoliation Syndrome ◽  
Cell Area ◽  
Corneal Endothelial Cells ◽  
Hexagonal Cell ◽  
Significant Group ◽  
Cell Ratio

Abstract Purpose: To compare early postoperative effects of uncomplicated phacoemulsification surgery on corneal endothelial cells and thickness in patients with pseudoexfoliation syndrome (PEX).Methods: One eye each of 32 patients with PEX and 32 age-matched non-PEX subjects was evaluated preoperatively and on 1st, 7th, and 30th days after uncomplicated phacoemulsification surgery in this retrospective case-control study. Nuclear firmness, corneal edema (CE), anterior chamber reaction (ACR) intensity were graded by a slit-lamp microscope. Endothelial cell density (ECD), coefficient of variation in cell area (CV), hexagonal cell ratio (HEX), and central corneal thickness (CCT) were measured using a noncontact specular microscope.Results: There was no significant group-difference in age, sex, corneal edema (CE), anterior chamber reaction (ACR), coefficient of variation in cell area (CV), and hexagonal cell ratio (HEX). Mean effective phaco time (EPT) was significantly lower intraoperatively (p<0.001) and logarithm of the minimum angle of resolution (logMAR) values of best-corrected visual acuity (BCVA) were significantly higher on both 1st (p<0.001), 7th (p=0.011), and 30th (p=0.025) days postoperatively in the PEX group than in the non-PEX group. Mean ECD was significantly lower in the PEX group than in the non-PEX group on 7th (p=0.013), and 30th (p=0.037) days postoperatively. The mean CCT significantly differed only on 1st (p<0.001) day postoperatively.Conclusion: Eyes with PEX presented lower corneal ECD and decreased BCVA after uncomplicated phacoemulsification surgery. Further, there was no association between CCT and PEX existence preoperatively and in the early postoperative period.

scholarly journals Progressive cracking technique for phacoemulsification of superhard cataracts: a case report

2019 ◽  
Vol 6 (1) ◽  
Author(s):  
Yun-e Zhao ◽  
Zhangliang Li ◽  
Pingjun Chang ◽  
Dandan Wang ◽  
Man Hu
Keyword(s):  
Endothelial Cells ◽  
Visual Acuity ◽  
Case Report ◽  
Corneal Edema ◽  
Corneal Endothelial Cell ◽  
Low Density ◽  
Corneal Endothelial Cells ◽  
Case Presentation ◽  
Finger Counting ◽  
Initial Learning

Abstract Background Complete nuclear disassembly of superhard cataracts cannot always be achieved by phaco chop, which is considered one of the best techniques for dealing with hard cataracts. We present a phaco chop-progressive cracking technique to divide superhard cataracts completely. Case presentation We presented a case of cataract with over Grade V nucleus sclerosis and very low density of corneal endothelial cell (812 cells/mm2). By performing the cataract surgery with our phaco chop-progressive cracking technique, the corneal endothelial cells were well protected and the patient’s visual acuity was markedly improved from finger counting at 40 cm to 20/200 the day after surgery without obvious corneal edema. Conclusions Although an initial learning curve was needed, this phaco chop-progressive cracking technique could be of particular benefit to the superhard cataract, especially in patients with low density of corneal endothelial cells.

scholarly journals SIRT1 Activation Using CRISPR/dCas9 Promotes Regeneration of Human Corneal Endothelial Cells through Inhibiting Senescence

Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1085
Author(s):  
Hye Jun Joo ◽  
Dae Joong Ma ◽  
Jin Sun Hwang ◽  
Young Joo Shin
Keyword(s):  
Endothelial Cells ◽  
Corneal Transplantation ◽  
Corneal Edema ◽  
Corneal Endothelial Cells ◽  
Sprague Dawley ◽  
Human Corneal Endothelial Cells ◽  
Sprague Dawley Rats ◽  
Associated Proteins ◽  
Activation Therapy

Human corneal endothelial cells (hCECs) are restricted in proliferative capacity in vivo. Reduction in the number of hCEC leads to persistent corneal edema requiring corneal transplantation. This study demonstrates the functions of SIRT1 in hCECs and its potential for corneal endothelial regeneration. Cell morphology, cell growth rates and proliferation-associated proteins were compared in normal and senescent hCECs. SIRT1 was activated using the CRISPR/dCas9 activation system (SIRT1a). The plasmids were transfected into CECs of six-week-old Sprague–Dawley rats using electroporation and cryoinjury was performed. Senescent cells were larger, elongated and showed lower proliferation rates and lower SIRT1 levels. SIRT1 activation promoted the wound healing of CECs. In vivo transfection of SIRT1a promoted the regeneration of CECs. The proportion of the S-phase cells was lower in senescent cells and elevated upon SIRT1a activation. SIRT1 regulated cell proliferation, proliferation-associated proteins, mitochondrial membrane potential, and oxidative stress levels. In conclusion, corneal endothelial senescence is related with a decreased SIRT1 level. SIRT1a promotes the regeneration of CECs by inhibiting cytokine-induced cell death and senescence. Gene function activation therapy using SIRT1a may serve as a novel treatment strategy for hCEC diseases.

scholarly journals Long-term Observation After Transplantation of Cultured Human Corneal Endothelial Cells for Corneal Endothelial Dysfunction

2021 ◽  
Author(s):  
Peng Sun ◽  
Lin Shen ◽  
Yuanbin Li ◽  
Liqun Du ◽  
Xinyi Wu
Keyword(s):  
Stem Cells ◽  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Conditioned Medium ◽  
Cell Transplantation ◽  
Adipose Derived Stem Cells ◽  
Corneal Endothelial Cells ◽  
Corneal Endothelial Dysfunction ◽  
Long Term Observation

Abstract Background At present, corneal transplantation is still the only way to treat serious corneal diseases caused by corneal endothelial dysfunction. However, the shortage of donor cornea tissues and human corneal endothelial cells (HCECs) remains a worldwide challenge. We cultivated HCECs by the use of a conditioned medium from orbital adipose-derived stem cells (OASC-CM) in vitro. Then the HCECs were used to treat animal corneal endothelial dysfunction models via cell transplantation. The initial effect was gratifying. The purpose of this study was to conduct a long-term observation and evaluation after cell transplantation. Methods First, orbital adipose-derived stem cells (OASCs) were isolated to prepare conditioned medium (CM). Then HCECs were cultivated and expanded by the usage of CM (CM-HCECs). Related CEC markers were analyzed by immunofluorescence. Cells proliferation ability was also tested. CM-HCECs were then transplanted into monkey corneal endothelial dysfunction models by cell injection. We carried out a 24-month postoperative preclinical observation and verified the long-term effect by histological examination and transcriptome sequencing. Results CM-HCECs expressed HCEC related markers and maintained polygonal cell morphology after several passages. During 24 months of cell transplantation into the monkey's anterior chamber, the cornea thickness and transparency kept healthy status, and the corneal endothelial cell density remained in the normal range. Gene sequencing showed that the gene expression pattern of CM-HCECs was similar to that of transplanted cells and HCECs. Conclusions The proliferation and repair ability of HCECs were significantly improved due to the effect of OASC-CM. The result of this study confirmed long-term therapeutic efficacy of CM-HCECs in vivo. Our research provided an extensive cell source and a promising prospect for regenerative medicine and cell-based therapy.

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