The Eye: Window to the Brain
The eyes are composed of many parts that together, sense and interpret light, enabling the formation of images via the brain. The front of the eye is called the cornea, and it is responsible for focusing light on the retina at the back of the eye. The retina contains a single layer epithelium, called the retinal pigment epithelium, which houses light sensing cells called rods and cones. The colored part of the eye, the iris, surrounds the pupil, which controls the amount of light that hits the lens, the part of the eye that sits directly behind the pupil. The lens enhances the focus of light on the retina, where the rods and cones convert the light into a chemical relay to the brain via the optic nerve. The results are the images we see.
See the Difference with Lifeline® Human Corneal Epithelial Cells
The eye is a sensitive organ and is quite exposed. To combat the external environment, an epithelial layer protects the outer cornea, providing a barrier against pathogens and foreign substances. These corneal epithelial cells are offered by Lifeline® for your research needs. Lifeline® human corneal epithelial cells are optimized for growth in OcuLife™ corneal epithelial medium for at least three passages. Read more below about a new reference for our corneal epithelial cells.
Ocular hypertension occurs when the intraocular pressure in the eye is higher than normal. Ocular hypertension is a major risk factor for glaucoma, which causes blindness. Although ocular hypertension is caused by a number of factors, it can be caused by exposure to glucocorticoids, often as a result of steroid-based treatments. Patients who experience this response are termed “steroid responders”. Patients with primary open-angle glaucoma commonly develop ocular hypertension following glucocorticoid exposure, and patients without glaucoma who develop glucocorticoid-induced ocular hypertension are at increased risk for glaucoma.
In a 2015 study, Jeong and colleagues performed a genome-wide association study (GWAS) to determine whether they could identify genes associated with glucocorticoid-induced ocular hypertension in patients who are steroid responders. They identified two single nucleotide polymorphisms (SNPs), both associated with the HCG22 gene. To confirm the presence of the HCG22 transcript in the eye, the authors performed RT-PCR in Lifeline® human corneal epithelial (HCE) cells and trabecular meshwork (TBM) cells. They found that HCG22 was expressed in both HCE and TBM cells, and in TBM cells, was stimulated by interleukin-1b treatment, and inhibited by triamcinolone acetonide (a steroid), and transforming growth factor-beta (TGF-b).
Since the function of HCG22 is relatively unknown and the SNPs identified in the GWAS are located upstream of the HCG22 promoter, the authors investigated how these SNPs might alter potential transcription factor binding. Interestingly, they found that one predicted effect was disrupted binding of the glucocorticoid receptor, which binds glucocorticoids and acts as a transcription factor. Finally, the researchers performed some analyses related to the HCG22 protein. They found that HCG22 is a 70-75 kDa mucin protein that is O-glycosylated and exported from the cell. Together, their results suggest that the SNPs in the novel mucin gene, HCG22, may result in dysregulation of HCG22 expression in the presence of glucocorticoids, leading to glucocorticoid-induced ocular hypertension. This type of SNP analysis may lead to predictive approaches to determine whether patients are at risk for ocular hypertension before receiving treatment.
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