Thermal stress induces dysfunction and facilitates senescence via disruption of cytoskeletal rearrangement and stimulation of the inflammatory response in primary endothelial cells

Abstract BackgroundThermal injury occurs when energy is transferred from a heat source to the body, causing local tissues to heat up. It has been demonstrated that the tissue temperature exceeds a certain threshold by exposure to external heat (thermal stress, TS), irreversible cell damage occurs, resulting in a delayed neovascularization. In recent years, warm paste is a popular item for people to keep warm in winter. Although the average temperature from the hot paste is only 54 ± 3°C, numerous cases of contact burns, that induced an increased capillary permeability in damaged tissue, by body warm paste were reported in our hospital.MethodsHerein, we evaluated the damage to primary microvascular endothelial cells (ECs) at 45°C with various times and demonstrated that exposure to TS at 45°C only for 10 minutes induced irreversible damage in ECs via suppressed proliferation and promoted apoptosis.ResultsTS significantly delayed the cell cycle and facilitated senescence in primary ECs. ECs exposed to TS lost their motility, and cytoskeletal rearrangement resulted in impaired angiogenic function. Furthermore, the result from mRNA array revealed that TS induced not only a negative regulation of migration and branching structures, but also revealed that TS exposure promoted apoptotic processes and TNF signalling resulting in increased expression of pro-inflammatory factors, such as IL-1β and IL-6.ConclusionTaken together, our results indicate that burn injury may initiate systemic injury of the vascular system even at 45°C only for 10 minutes, which might be one of the mechanisms of delayed damaged tissue repair.Trial registrationNot applicable.