The wound healing response within corneal epithelium cells is controlled by the purinergic P2X7 receptor, purinergic P2Y2 receptor, and Pannexin1 transmembrane proteins. The response is initiated by the release of ATP into the extracellular space by damaged cells and by the Pannexin1 channel protein and limited by the hydrolysis of extracellular ATP by ecto-ATPases. P2X7 and P2Y2 receptors are necessary for the initiation of cell migration, actin reorganization, and cell to cell communication required for the sheet like migration found within the corneal epithelium wound response. ARL 67156 Trisodium Salt Hydrate, an inhibitor for human and murine ecto-ATPases, was used to inhibit the hydrolysis of extracellular ATP during the wound response to prolong and further elevate extracellular ATP concentrations to increase the cellular activity and cell to cell communication of the wound response. The goal was to compare primary diabetic murine and human cells. However, there were issues with culturing these cells and diabetic murine and non-diabetic primary and established human cells were used for these experiments. Significant increases in cellular activity were found in both primary human cells with a 100 ARL to 10 ATP concentration ratio while no significant changes in cellular activity were found with the murine diabetic cells at any ARL concentration. In summary, with increased ATP in the wound response due to the inhibition of hydrolysis enzymes, human cells displayed increased levels and rates of cell-to-cell communication during the delayed wound response. / 2024-01-27T00:00:00Z
| Identifer | oai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/45529 |
| Date | 27 January 2023 |
| Creators | Azzari, Nicholas A. |
| Contributors | Trinkaus-Randall, Vickery |
| Source Sets | Boston University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis/Dissertation |
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