scholarly journals Receptor interacting protein 3 kinase, not 1 kinase, through MLKL-mediated necroptosis is involved in UVA-induced corneal endothelium cell death

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Zhen Yu ◽  
Nikolaos E. Efstathiou ◽  
Victor S. M. C. Correa ◽  
Xiaohong Chen ◽  
Kenji Ishihara ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Death ◽  
Corneal Endothelium ◽  
Tissue Injury ◽  
Ex Vivo ◽  
Solar Spectrum ◽  
Corneal Endothelial Cells ◽  
Interacting Protein ◽  
Uva Irradiation ◽  
Culture Model

AbstractUltraviolet (UV) is one of the most energetic radiations in the solar spectrum that can result in various tissue injury disorders. Previous studies demonstrated that UVA, which represents 95% of incident photovoltaic radiation, induces corneal endothelial cells (CECs) death. Programmed cell death (PCD) has been implicated in numerous ophthalmologic diseases. Here, we investigated receptor-interacting protein 3 kinase (RIPK3), a key signaling molecule of PCD, in UVA-induced injury using a short-term corneal endothelium (CE) culture model. UVA irradiation activated RIPK3 and mediated necroptosis both in mouse CE and primary human CECs (pHCECs). UVA irradiation was associated with upregulation of key necroptotic molecules (DAI, TRIF, and MLKL) that lie downstream of RIPK3. Moreover, RIPK3 inhibition or silencing in primary corneal endothelial cells suppresses UVA-induced cell death, along with downregulation of MLKL in pHCECs. In addition, genetic inhibition or knockout of RIPK3 in mice (RIPK3K51A and RIPK3−/− mice) similarly attenuates cell death and the levels of necroptosis in ex vivo UVA irradiation experiments. In conclusion, these results identify RIPK3, not RIPK1, as a critical regulator of UVA-induced cell death in CE and indicate its potential as a future protective target.

Effect of Cysteamine on Oxidative Stress-induced Cell Death of Human Corneal Endothelial Cells

2011 ◽  
Vol 36 (10) ◽  
pp. 910-917 ◽  
Author(s):  
Young Joo Shin ◽  
Jong Mo Seo ◽  
Tae Young Chung ◽  
Joon Young Hyon ◽  
Won Ryang Wee
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Cell Death ◽  
Corneal Endothelial Cells ◽  
Human Corneal Endothelial Cells

scholarly journals The Effect of Phacoemulsification on Corneal Endothelial Cells Morphology and Thickness

2020 ◽  
Vol 36 (4) ◽  
Author(s):  
Abd Elaziz Mohamed Elmadina ◽  
Raghda Faisal Abdelfatah ◽  
Saif Hassan Alrasheed ◽  
Mustafa Abdu ◽  
Manzoor Ahmad Qureshi
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Density ◽  
Corneal Endothelium ◽  
Central Corneal Thickness ◽  
Corneal Thickness ◽  
Endothelial Cell Density ◽  
P Value ◽  
Corneal Endothelial Cells ◽  
Before And After

Purpose:  To compare the corneal endothelial cells morphology and central corneal thickness (CCT) before and after phacoemulsification in Sudanese population. Place and Duration of Study:  Al-Neelain eye hospital, Khartoum, Sudan, from January 2018 to May 2018. Study Design:  Observational longitudinal study. Methods:  One hundred and forty eyes of 140 patients with immature senile cataract were selected by convenient sampling. The age ranged from 40 to 85 years. The patients underwent complete ocular examination including morphology of corneal endothelial cells and CCT using computerized non-contact specular microscope. Inclusion criteria for the study was eyes with normal corneal endothelial cells and cell density more than 1000 cells/mm2. We excluded patients with ocular or systemic diseases, previous history of intraocular surgery, refractive surgery or trauma as well as contact lenses wear. The patients underwent phacoemulsification by a single surgeon. The examination parameters were repeated one month after surgery. Descriptive and comparative statistical analyses were performed using SPSS for Windows Version 21.0. Results:  There was significant reduction in mean endothelial cells density after phacoemulsification compared to baseline with p < 0.001. There was also significant post-operative reduction in mean endothelial cells number as compared to baseline (P value < 0.001). Mean endothelial cells hexagonality was reduced after surgery with P value of 0.003. No significant difference was found between mean coefficient variation of endothelial cells size before and after phacoemulsification (P = 0.55). Central corneal thickness showed significant increase post-operatively, P = 0.003. Conclusion:  Phacoemulsification causes significant damage to corneal endothelium cells, including decrease in corneal endothelial cell density, hexagonality and cell number. Key Words:  Corneal endothelium, Endothelial cell density, Central corneal thickness, Phacoemulsification.

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 Myh11 Lineage Corneal Endothelial Cells and ASCs Populate Corneal Endothelium

2019 ◽  
Vol 60 (15) ◽  
pp. 5095 ◽  
Author(s):  
Bruce A. Corliss ◽  
H. Clifton Ray ◽  
Corbin Mathews ◽  
Kathleen Fitzgerald ◽  
Richard W. Doty ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Corneal Endothelium ◽  
Corneal Endothelial Cells

scholarly journals Extracellular Vesicles Derived From Human Corneal Endothelial Cells Inhibit Proliferation of Human Corneal Endothelial Cells

2021 ◽  
Author(s):  
Mohit Parekh ◽  
Hefin Rhys ◽  
Tiago Ramos ◽  
Stefano Ferrari ◽  
Sajjad Ahmad
Keyword(s):  
Endothelial Cells ◽  
Extracellular Vesicles ◽  
Ex Vivo ◽  
Treatment Options ◽  
Proliferative Capacity ◽  
Corneal Endothelial Cells ◽  
Human Corneal Endothelial Cells ◽  
The Media

Abstract Corneal endothelial cells (CEnCs) are a monolayer of hexagonal cells that are responsible for maintaining the function and transparency of the cornea. Damage or dysfunction of CEnCs could lead to blindness. Human CEnCs (HCEnCs) have shown limited proliferative capacity in vivo hence, their maintenance is crucial. Extracellular vesicles (EVs), are responsible for inter- and intra-cellular communication, proliferation, cell-differentiation, migration, and many other complex biological processes. Therefore, we investigated the effect of EVs (derived from human corneal endothelial cell line – HCEC-12) on corneal endothelial cells. HCEC-12 cells were starved with serum-depleted media for 72 hours. The media was ultracentrifuged at 100,000xg to isolate the EVs. EV counting, characterization, internalization and localization were performed using NanoSight, flow cytometry, Dil labelling and confocal microscopy respectively. HCEC-12 and HCEnCs were cultured with media supplemented with EVs. Extracted EVs showed a homogeneous mixture of exosomes and microvesicles. Cells with EVs decreased the proliferation rate; increased apoptosis and cell size; showed poor wound healing response in vitro and on ex vivo human, porcine, and rabbit CECs. Thirteen miRNAs were found in the EV sample using next generation sequencing. We observed that increased cellular uptake of EVs by CECs limit the proliferative capacity of HCEnCs. These preliminary data may help in understanding the pathology of corneal endothelial dysfunction and provide further insights in the development of future therapeutic treatment options.

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