scholarly journals Blue Light Induces Impaired Autophagy through Nucleotide-Binding Oligomerization Domain 2 Activation on the Mouse Ocular Surface

2021 ◽  
Vol 22 (4) ◽  
pp. 2015
Author(s):  
Ying Li ◽  
Rujun Jin ◽  
Lan Li ◽  
Ji Suk Choi ◽  
Jonghwa Kim ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Blue Light ◽  
Ocular Surface ◽  
Light Exposure ◽  
Reactive Oxygen ◽  
Nucleotide Binding ◽  
Oxygen Species ◽  
Knock Out ◽  
Corneal Epithelial ◽  
Oligomerization Domain

In this study, we investigated the effects of blue light exposure on nucleotide-binding oligomerization domain 2 (NOD2) expression on the mouse ocular surface and evaluated the role of NOD2 activation in light-induced cell death. Mice were divided into wild-type (WT), NOD2-knock out (KO), WT + blue light (WT + BL), and NOD2-KO + blue light (NOD2-KO + BL) groups, and the mice in the WT+BL and NOD2-KO + BL groups were exposed to blue light for 10 days. After 10 days of blue light exposure, increased reactive oxygen species and malondialdehyde were observed in the WT + BL and NOD2-KO + BL groups, and the WT + BL group showed a higher expression of NOD2 and autophagy related 16 like 1. Although both WT+BL and NOD2-KO + BL groups showed an increase in the expression of light chain 3-II, NOD2-KO + BL mice had a significantly lower p62 expression than WT + BL mice. In addition, NOD2-KO+BL mice had significantly lower corneal epithelial damage and apoptosis than WT + BL mice. In conclusion, blue light exposure can induce impaired autophagy by activation of NOD2 on the ocular surface. In addition, the reactive oxygen species (ROS)–NOD2–autophagy related 16 like 1 (ATG16L) signaling pathway may be involved in the blue-light-induced autophagy responses, resulting in corneal epithelial apoptosis.

scholarly journals Absence of the NOD2 protein renders epithelia more susceptible to barrier dysfunction due to mitochondrial dysfunction

2017 ◽  
Vol 313 (1) ◽  
pp. G26-G38 ◽  
Author(s):  
Alpana Saxena ◽  
Fernando Lopes ◽  
Karen K. H. Poon ◽  
Derek M. McKay
Keyword(s):  
Reactive Oxygen Species ◽  
Barrier Function ◽  
Paneth Cell ◽  
Metabolic Stress ◽  
Reactive Oxygen ◽  
Nucleotide Binding ◽  
Intracellular Bacteria ◽  
Oxygen Species ◽  
E Coli ◽  
Oligomerization Domain

Irregular mitochondria structure and reduced ATP in some patients with IBD suggest that metabolic stress contributes to disease. Loss-of-function mutation in the nucleotide-binding oligomerization domain (NOD)-2 gene is a major susceptibility trait for IBD. Hence, we assessed if loss of NOD2 further impairs the epithelial barrier function instigated by disruption of mitochondrial ATP synthesis via the hydrogen ionophore dinitrophenol (DNP). NOD2 protein (virtually undetectable in epithelia under basal conditions) was increased in T84 (human colon cell line) cells treated with noninvasive Escherichia coli + DNP (16 h). Increased intracellular bacteria in wild-type (WT) and NOD2 knockdown (KD) cells and colonoids from NOD2−/− mice were mediated by reactive oxygen species (ROS) and the MAPK ERK1/2 pathways as determined by cotreatment with the antioxidant mitoTEMPO and the ERK inhibitor U0126: ROS was upstream of ERK1/2 activation. Despite increased E. coli in DNP-treated NOD2 KD compared with WT cells, there were no differences in the internalization of fluorescent inert beads or dead E. coli particles. This suggests that lack of killing in the NOD2 KD cells was responsible for the increased numbers of viable intracellular bacteria; a conclusion supported by evidence of reduced autophagy in NOD2 KD T84 epithelia. Thus, in a two-hit hypothesis, decreased barrier function due to dysfunctional mitochondrial is amplified by lack of NOD2 in transporting enterocytes: subsequently, greater numbers of bacteria entering the mucosa would be a significant inflammatory threat especially since individuals with NOD2 mutations have compromised macrophage and Paneth cell responses to bacteria. NEW & NOTEWORTHY Increased internalization of bacteria by epithelia with dysfunctional mitochondria (reduced ATP) is potentiated if the cells lack nucleotide-binding oligomerization domain 2 (NOD2), mutations in which are inflammatory bowel disease-susceptibility traits. Uptake of bacteria was dependent on reactive oxygen species and MAP-kinase activity, and the increased viable intracellular bacteria in NOD2−/− cells likely reflect a reduced ability to recognize and kill bacteria. Thus a significant barrier defect occurs with NOD2 deficiency in conjunction with metabolic stress that could contribute to inflammation.

Therapeutic Contact Lens for Scavenging Excessive Reactive Oxygen Species on the Ocular Surface

ACS Nano ◽  
2020 ◽  
Vol 14 (2) ◽  
pp. 2483-2496 ◽  
Author(s):  
Seung Woo Choi ◽  
Bong Geun Cha ◽  
Jaeyun Kim
Keyword(s):  
Reactive Oxygen Species ◽  
Contact Lens ◽  
Ocular Surface ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals An Immunohistochemical Study of the Increase in Antioxidant Capacity of Corneal Epithelial Cells by Molecular Hydrogen, Leading to the Suppression of Alkali-Induced Oxidative Stress

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Cestmir Cejka ◽  
Jan Kossl ◽  
Vladimir Holan ◽  
John H. Zhang ◽  
Jitka Cejkova
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Antioxidant Capacity ◽  
Molecular Hydrogen ◽  
Reactive Oxygen ◽  
Corneal Neovascularization ◽  
Scar Formation ◽  
Oxygen Species ◽  
Buffer Solution ◽  
Corneal Epithelial

Corneal alkali burns are potentially blinding injuries. Alkali induces oxidative stress in corneas followed by excessive corneal inflammation, neovascularization, and untransparent scar formation. Molecular hydrogen (H2), a potent reactive oxygen species (ROS) scavenger, suppresses oxidative stress and enables corneal healing when applied on the corneal surface. The purpose of this study was to examine whether the H2 pretreatment of healthy corneas evokes a protective effect against corneal alkali-induced oxidative stress. Rabbit eyes were pretreated with a H2 solution or buffer solution, by drops onto the ocular surface, and the corneas were then burned with 0.25 M NaOH. The results obtained with immunohistochemistry and pachymetry showed that in the corneas of H2-pretreated eyes, slight oxidative stress appeared followed by an increased expression of antioxidant enzymes. When these corneas were postburned with alkali, the alkali-induced oxidative stress was suppressed. This was in contrast to postburned buffer-pretreated corneas, where the oxidative stress was strong. These corneas healed with scar formation and neovascularization, whereas corneas of H2-pretreated eyes healed with restoration of transparency in the majority of cases. Corneal neovascularization was strongly suppressed. Our results suggest that the corneal alkali-induced oxidative stress was reduced via the increased antioxidant capacity of corneal cells against reactive oxygen species (ROS). It is further suggested that the ability of H2 to induce the increase in antioxidant cell capacity is important for eye protection against various diseases or external influences associated with ROS production.

scholarly journals Intra- and extracellular reactive oxygen species generated by blue light

2006 ◽  
Vol 77A (3) ◽  
pp. 470-477 ◽  
Author(s):  
Y. Omata ◽  
J.B. Lewis ◽  
S. Rotenberg ◽  
P.E. Lockwood ◽  
R.L.W. Messer ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Blue Light ◽  
Reactive Oxygen ◽  
Oxygen Species
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