Type II diabetes is a major cause of blindness according to the World Health Organization (WHO, 2018). Diabetics are at risk of developing corneal diseases such as recurrent abrasions, ulcers, and erosions due to dysfunctional wound healing. Corrective surgeries or corneal transplants may be considered as a treatment in some, but not all, cases. The purinoreceptor P2X7 has been shown to be involved in cell-cell communication and in the restructuring of cytoskeletal actin, a necessary process for cell migration in wound healing. P2X7 relies on the binding of extracellular ATP for activation. Panx1 is a transmembrane protein whose primary role is for the release of intracellular ATP into the extracellular space. In healthy corneal epithelium, Panx1 localizes to the wound edge and forms clusters with the P2X7, which augments the wound healing response. This thesis looks at the localization of Panx1 in pre-diabetic murine corneal tissue. It was found that Panx1 is less expressed and does not localize to the wound edge to the extent as control corneas, therefore, creating less clusters with P2X7. Furthermore, preliminary studies that inhibit Panx1 with probenecid reduce the communication between cells, which is hypothesized as critical for migration of the tissue sheet and proper wound healing. / 2019-12-17T00:00:00Z
| Identifer | oai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/36710 |
| Date | 17 June 2019 |
| Creators | Rhodes, Garrett |
| Contributors | Trinkaus-Randall, Vickery |
| Source Sets | Boston University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis/Dissertation |
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