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Glucocorticoid Receptor Signaling is Critical for Mouse Corneal Development, Inhibition of Inflammatory Response and Neovascularization of the Cornea

ABSTRACT: Glucocorticoid Receptor Signaling is Critical for Mouse Corneal Development, Inhibition of Inflammatory Response and Neovascularization of the Cornea

PROVIDER: PRJNA882031 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21626687_1.fastq.gz	Fastqsanger.gz
	SRR21626687_2.fastq.gz	Fastqsanger.gz
	SRR21626688_1.fastq.gz	Fastqsanger.gz
	SRR21626688_2.fastq.gz	Fastqsanger.gz
	SRR21626689_1.fastq.gz	Fastqsanger.gz

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Project description:The cornea is the transparent tissue at the forefront of the eye. Its outermost layer, the corneal epithelium, acts as a protective barrier for the ocular chamber. The cornea is avascular and its homeostasis relies on alternative sources to receive nutrients and growth factors, essential for maintaining its physiological functions and transparency. These sources include the corneal epithelium itself, the innervation and the tear film, collectively forming the corneal microenvironment. Any disruption to this finely balanced system (due to injury, ageing or diseases) can impair corneal transparency and lead to a progressive opacification, ultimately resulting in vision loss. Corneal blindness affects over 28 million people worldwide and represents the fourth leading cause of blindness. Among corneal injuries, abrasions are defined by a transient disruption in the integrity and cohesion of the epithelial barrier and are the most common type of eye injury encountered in clinical practice. Abrasion triggers a complex corneal wound healing process, involving the whole microenvironment, essential to restore transparency. However, a delayed or defective healing can lead to severe complications and visual impairments. Frequently caused by traumatic events, abrasion is also a mandatory step for some refractive surgeries such as photorefractive keratectomy (PRK). Understanding the molecular mechanisms underlying corneal wound healing is thus critical to improve the clinical outcomes and minimize the risk of complications such as haze or delayed epithelial regeneration. The aim of this study is to characterize the temporal dynamics of the tear fluid proteome following PRK and identify molecular signatures associated with corneal epithelial healing. We conducted a prospective cohort study involving longitudinal proteomic analysis of tear samples with mass spectrometry at baseline (preoperative), 30 minutes postoperatively (day 0), and on day 3 after PRK. Ten healthy adult patients undergoing bilateral PRK for myopia correction were included in this study. Corneal epithelial injury was induced by bilateral PRK, a standardized surgical model of epithelial removal followed by laser ablation.

Dataset Information

Glucocorticoid Receptor Signaling is Critical for Mouse Corneal Development, Inhibition of Inflammatory Response and Neovascularization of the Cornea

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