Aberrations in Cell Signaling Quantified in Diabetic Murine Globes after Injury
Nicholas A. Azzari,
Kristen L. Segars,
Srikar Rapaka,
Landon Kushimi,
Celeste B. Rich,
Vickery Trinkaus-Randall
Affiliations
Nicholas A. Azzari
Department of Biochemistry and Cell Biology, Boston University Chobanian and Avedisian School of Medicine, 72 E. Concord St., Boston, MA 02118, USA
Kristen L. Segars
Department of Pharmacology, Physiology and Biophysics, Boston University Chobanian and Avedisian School of Medicine, 72 E. Concord St., Boston, MA 02118, USA
Srikar Rapaka
Department of Medicine, Boston University Chobanian and Avedisian School of Medicine, 72 E. Concord St., Boston, MA 02118, USA
Landon Kushimi
Department of Computer Science, Center for Computing and Data Sciences, Boston University, 665 Commonwealth Ave, Boston, MA 02115, USA
Celeste B. Rich
Department of Biochemistry and Cell Biology, Boston University Chobanian and Avedisian School of Medicine, 72 E. Concord St., Boston, MA 02118, USA
Vickery Trinkaus-Randall
Department of Biochemistry and Cell Biology, Boston University Chobanian and Avedisian School of Medicine, 72 E. Concord St., Boston, MA 02118, USA
The corneal epithelium is an avascular structure that has a unique wound healing mechanism, which allows for rapid wound closure without compromising vision. This wound healing mechanism is attenuated in diabetic patients, resulting in poor clinical outcomes and recurrent non-healing erosion. We investigated changes in cellular calcium signaling activity during the wound response in murine diabetic tissue using live cell imaging from both ex vivo and in vitro models. The calcium signaling propagation in diabetic cells was significantly decreased and displayed altered patterns compared to non-diabetic controls. Diabetic cells and tissue display distinct expression of the purinergic receptor, P2X7, which mediates the wound healing response. We speculate that alterations in P2X7 expression, interactions with other proteins, and calcium signaling activity significantly impact the wound healing response. This may explain aberrations in the diabetic wound response.
