Priya Mistry
1 media/Priya Mistry screen_thumb.PNG 2020-05-05T22:38:39+00:00 Schmid College of Science and Technology ef61ed75d203ace65a2b05613a8adc7a45c04b00 18 1 B.S. Biochemistry & Molecular BiologyMinor: Law, Justice, & Social Control
Mentor: Dr. Ajay Sharma plain 2020-05-05T22:38:39+00:00 Schmid College of Science and Technology ef61ed75d203ace65a2b05613a8adc7a45c04b00
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Priya Mistry
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Overview: Our research demonstrates that an increase in osmolarity could cause release of proinflammatory cytokines on human ocular surface epithelial cells, which would contribute to the ocular surface damage associated with dry eye.
Comparative Analysis of Hyperosmotic Stress-mediated Modulation of Cytokine Gene Expression in Human Conjunctival and Corneal Epithelial Cells
Abstract: Increase in tear osmolarity and chronic inflammation are cardinal feature of dry eye disease. The ocular surface is covered by conjunctival and corneal epithelial cells. Exposure of ocular surface epithelial cells to hyperosmolar stress may initiate inflammatory response. Therefore, the present study was designed to investigate the differential changes in the gene expression of proinflammatory cytokines in human conjunctival and corneal epithelial cells upon exposure to hyperosmolar stress. The cultured human corneal and conjunctival epithelial cells were exposed to hyperosmolar stress for 12 and 24 hours. The mRNA was isolated from these cells and was reverse transcribed into cDNA. The cDNA was used for quantification of IL1, IL6 and TNFα gene expression by real-time PCR. Hyperosmotic stress caused a 1.5- and 2-fold increase in the gene expression of IL1 in the human conjunctival and corneal epithelial cells respectively. Hyperosmotic stress also caused a 3- 4 fold increase in IL6 expression in conjunctival cells, whereas the increase in IL6 gene expression was much more robust in human corneal epithelial cells. Similarly, hyperosmotic stress caused a 2-3 fold increase in TNFα in human conjunctival cells, whereas a >10-fold increase in TNFα expression was observed in the human corneal epithelial cells. Our data suggests that hyperosmolar stress causes an increase in the gene expression of proinflammatory cytokines in cultured human corneal and conjunctival epithelial cells. Corneal epithelial cells seem to be more sensitive to the detrimental effect of hyperosmotic stress. The hyperosmolar stress-mediated increase in proinflammatory cytokine milieu may be partly responsible for dry eye associated chronic low grade inflammation.
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