Department of Biochemistry and Cell Biology, Boston University Chobanian and Avedisian School of Medicine, 72 E. Concord St., Boston, MA 02118, USA.
Department of Pharmacology, Physiology and Biophysics, Boston University Chobanian and Avedisian School of Medicine, 72 E. Concord St., Boston, MA 02118, USA.
Cells. 2023 Dec 21;13(1):26. doi: 10.3390/cells13010026.
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.
角膜上皮是一种无血管的结构，具有独特的伤口愈合机制，可在不影响视力的情况下实现快速伤口闭合。糖尿病患者的这种伤口愈合机制减弱，导致临床效果不佳和反复不愈合的侵蚀。我们使用离体和体外模型的活细胞成像，研究了在小鼠糖尿病组织的伤口反应过程中细胞钙信号转导活性的变化。与非糖尿病对照相比，糖尿病细胞中的钙信号转导明显减少，并呈现出不同的模式。糖尿病细胞和组织显示出嘌呤能受体 P2X7 的明显表达，该受体介导伤口愈合反应。我们推测，P2X7 表达的改变、与其他蛋白质的相互作用以及钙信号转导活性显著影响伤口愈合反应。这可能解释了糖尿病伤口反应的异常。
