Aberrations in Cell Signaling Quantified in Diabetic Murine Globes after Injury

Author:

Azzari Nicholas A.1,Segars Kristen L.2,Rapaka Srikar3,Kushimi Landon4,Rich Celeste B.1,Trinkaus-Randall Vickery125ORCID

Affiliation:

1. Department of Biochemistry and Cell Biology, Boston University Chobanian and Avedisian School of Medicine, 72 E. Concord St., Boston, MA 02118, USA

2. Department of Pharmacology, Physiology and Biophysics, Boston University Chobanian and Avedisian School of Medicine, 72 E. Concord St., Boston, MA 02118, USA

3. Department of Medicine, Boston University Chobanian and Avedisian School of Medicine, 72 E. Concord St., Boston, MA 02118, USA

4. Department of Computer Science, Center for Computing and Data Sciences, Boston University, 665 Commonwealth Ave, Boston, MA 02115, USA

5. Department of Ophthalmology, Boston University Chobanian and Avedisian School of Medicine, 72 E. Concord St., Boston, MA 02118, USA

Abstract

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.

Funder

National Institute of Health

Massachusetts Lions Eye Research Foundation

New England Corneal Transplant Fund

Publisher

MDPI AG

Subject

General Medicine

Reference68 articles.

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