2025, Vol. 29 ›› Issue (8): 1578-1584

Mechanism of Piezo-type mechanosensitive ion channel component 1 in rat pressure injury

Sun Jiaqi1, 2, Bian Lu1, Shi Wentao1, Wu Xuechao1, Lu Xiaojie1, 2   

Abstract: BACKGROUND: The mechanisms underlying the occurrence of pressure injuries are complex, and it is not entirely clear which factors play a central role in the development of pressure injuries and how these factors operate.
OBJECTIVE: To investigate the relationship between Piezo-type mechanosensitive ion channel component 1 (Piezo1) and the occurrence of pressure injuries.
METHODS: (1) Cellular experiment: Human immortalized keratinocytes (HaCaT) were treated with Yoda1, a Piezo1 agonist, at different concentrations. Cell viability, calcium ion influx, Piezo1, and apoptosis-related protein expression were detected. (2) Animal experiment: Twelve Sprague-Dawley rats were randomly divided into a control group and three experimental groups, with three rats in each group. The control group was not subjected to pressure, while in the three experimental groups, magnets with a thickness of 1, 2, and 3 mm were used to press on both sides of the rats’ back for 1 hour, respectively, to establish the animal models of pressure injuries. After modeling, all traumatic tissues were excised and subjected to hematoxylin-eosin, Masson, immunofluorescence staining and western blot assay.
RESULTS AND CONCLUSION: Cellular experiments: The results of live/dead cell staining showed that HaCaT cell apoptosis increased with the increase of Yoda1 concentration (0, 2.5, 5, and 10 μmol/L), and calcium ion influx increased with the increase of Yoda1 concentration (0, 5, and 10 μmol/L), as well as with the prolongation of treatment time. Western blot assay results showed an increase in the expression of BAX, TG2, and PIEZO1 and a decrease in the expression of the expression of Bcl-2 protein in HaCaT cells in 5 and 10 μmol/L Yoda1 groups compared with the control group (0 μmol/L Yoda1). Animal experiments: The results of hematoxylin-eosin and Masson staining showed that the skin structure of the three experimental groups was damaged at the compression site, there was subcutaneous fat liquefaction and necrosis, and collagen was sparse and disorganized, and damage to the skin structure at the compression site was aggravated with the increase of magnet thickness. Immunofluorescence staining and western blot results showed that compared with the control group, the expression of BAX, TG2, Yap1 and PIEZO1 proteins was elevated, and the expression of Bcl-2 proteins was lowered in the three experimental groups. Moreover, the expression of related proteins showed more significant changes with the increase of magnet thickness (pressure). To conclude, skin compression activates Piezo1, leading to a significant influx of calcium ions. As the pressure increases, this ultimately results in cell apoptosis due to calcium overload.
Key words: pressure injury, Piezo-type mechanosensitive ion channel component 1, PIEZO1, calcium overload, HaCaT cells