Hypoxia as pathogenic factor affecting the eye tissues: The selective apoptotic damage of the conjunctiva and anterior epithelium of the cornea

Akberova, S. I.; Markitantova, Yu. V.; Ryabtseva, A. A.; Stroeva, O. G.

doi:10.1134/s1607672916020198

Cited by 10 publications

(13 citation statements)

References 10 publications

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“…Apoptosis is an important mechanism in the development of dry eye. The apoptosis index of epithelial cells in dry eye is increased 49 . Dry eye is an immune disease, and apoptosis is involved in the development of immune cells, immune regulation, immune effect, and many other physiological and pathological processes 50 .…”

Section: Discussionmentioning

confidence: 99%

Air pollutant particulate matter 2.5 induces dry eye syndrome in mice

Tan

Yang

et al. 2018

Sci Rep

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In this study, we explored the effects of particulate matter 2.5 (PM2.5) eye drops on the ocular surface structure and tear function in mice and established a novel animal model for dry eye research. We found that, following treatment with PM2.5, the tear volume and, the tear film break-up time showed statistical differences at each time point (P < 0.05). The FL score of the PM2.5-treated group was higher than that of others (P < 0.05). The average number of corneal epithelial layer cells in groups A and B was significantly lower than that in group C (P < 0.05). Scanning electron microscopy and transmission electron microscopy revealed that the number of corneal epithelial microvilli and corneal desmosomes was drastically reduced in group C. PM2.5 induced apoptosis in the corneal superficial and basal epithelium and led to abnormal differentiation and proliferation of the ocular surface with higher expression levels of Ki67 and a reduced number of goblet cells in the conjunctival fornix in group C. PM2.5 significantly increased the levels of TNF-α, NF-κB p65 (phospho S536), and NF-κB in the cornea. Thus, the topical administration of PM2.5 in mice induces ocular surface changes that are similar to those of dry eye in humans, representing a novel model of dry eye.

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Section: Discussionmentioning

confidence: 99%

Air pollutant particulate matter 2.5 induces dry eye syndrome in mice

Tan

Yang

et al. 2018

Sci Rep

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“…Several conditions may result in corneal hypoxia, such as inflammation, diabetes, infection, dry eye, and limbal stem cell deficiency 7‐13 . TSP‐1 is an extracellular matrix protein interacting with various ligands including cell receptors, growth factors, cytokines, and proteases to regulate various physiological and pathological phenomena.…”

Section: Discussionmentioning

confidence: 99%

“…Several conditions may result in corneal hypoxia, such as inflammation, diabetes, infection, dry eye, and limbal stem cell deficiency. [7][8][9][10][11][12][13] TSP-1 is an extracellular matrix protein interacting with various ligands including cell receptors, growth factors, cytokines, and proteases to regulate various physiological and pathological phenomena. TSP-1 is regulated during ocular surface inflammation, injury, and hypoxia, 50 and is an important activator of latent TGF-β, thus, promoting immunomodulatory and wound healing functions.…”

Section: Hce-derived Exosomes Mediate Wound Healing and Cell-cell Amentioning

confidence: 99%

“…[4][5][6] Of note, several conditions may cause corneal hypoxia, such as inflammation, diabetes, infection, dry eye, and limbal stem cell deficiency. [7][8][9][10][11][12][13] Paraptosis is a type of programed cell death that occurs under certain physiological conditions including hypoxia. 14 It only requires caspase-9, is not associated with the release of cytochrome c and formation of apoptotic bodies, 15 and is characterized by cytoplasmic vacuolation.…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, decreased oxygen levels may lead to corneal neovascularization, resulting in decreased corneal transparency 4‐6 . Of note, several conditions may cause corneal hypoxia, such as inflammation, diabetes, infection, dry eye, and limbal stem cell deficiency 7‐13 …”

Section: Introductionmentioning

confidence: 99%

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Thrombospondin 1‐induced exosomal proteins attenuate hypoxia‐induced paraptosis in corneal epithelial cells and promote wound healing

Lai

Lee

et al. 2020

FASEB j.

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Thrombospondin‐1 (TSP1) is involved in corneal wound healing caused by chemical injury. Herein, we examined the effects of TSP1 on hypoxia‐induced damages and wound‐healing activity in human corneal epithelial (HCE) cells. Exosomal protein expression was determined using liquid chromatography‐tandem mass spectrometry, and HCE cell migration and motility were examined through wound‐healing assay and time‐lapse microscopy. Reestablishment of cell junctions by TSP1 was assessed through confocal microscopy and 3D image reconstruction. Our results show that CoCl2‐induced hypoxia promoted HCE cell death by paraptosis. TSP1 protected these cells against paraptosis by attenuating mitochondrial membrane potential depletion, swelling and dilation of endoplasmic reticulum and mitochondria, and mitochondrial fission. Exosomes isolated from HCE cells treated with TSP1 contained wound healing‐associated proteins that were taken up by HCE cells to promote tissue remodeling and repair. TSP1 protected HCE cells against hypoxia‐induced damages and inhibited paraptosis progression by promoting cell migration, cell‐cell adhesion, and extracellular matrix remodeling. These findings indicate that TSP1 ameliorates hypoxia‐induced paraptosis in HCE cells and promotes wound healing and remodeling by regulating exosomal protein expression. TSP1 may, therefore, play important roles in the treatment of hypoxia‐associated corneal diseases.

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Hypoxia adaptation in the cornea: Current animal models and underlying mechanisms

Pang

Lennikov

Yang

2021

Anim Models and Exp Med

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Hypoxia is a state when the oxygen supply does not meet the tissue's needs. Organisms, including mammals, have developed defense mechanisms to survive hypoxia, known as hypoxia adaptation. The hypoxia adaptation process has been studied in numerous tissues and diseases, including ischemia of the heart, brain, and nearly every major organ. Besides ischemia, aggressively malignant tumor 1 and systemic hypoxic status 2 are also the focus of hypoxia adaptation research. The eyes, being a unique and important sensory organ, impact greatly on a person's quality of life. The core concept of any visual system is refraction of the light into a photosensitive array (retina) and further processing into electrochemical signals for the brain neural networks to process and interpret. The eye developed a precise regulatory mechanism for each component to accomplish the visual cycle, a complex and energy-demanding function in a

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Hypoxia as pathogenic factor affecting the eye tissues: The selective apoptotic damage of the conjunctiva and anterior epithelium of the cornea

Cited by 10 publications

References 10 publications

Air pollutant particulate matter 2.5 induces dry eye syndrome in mice

Air pollutant particulate matter 2.5 induces dry eye syndrome in mice

Thrombospondin 1‐induced exosomal proteins attenuate hypoxia‐induced paraptosis in corneal epithelial cells and promote wound healing

Hypoxia adaptation in the cornea: Current animal models and underlying mechanisms

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