Abstract
Hip fracture is the most common type of injury in elderly people and is associated with a high incidence of complications and risk of mortality. In these patients, subsequent pulmonary infection can contribute to the development of an acute lung injury, a consequence of the systemic inflammatory response induced by hip fracture. Although the crucial role of microRNAs (miRNAs) in inflammatory responses has been established, the functions of miRNAs in the inflammatory responses associated with lung injury after hip fracture remain poorly understood. In this study, we explored the potential role of miR-205-5p in lung injury after hip fracture in an in vivo hip fracture model and in vitro cultures of human pulmonary alveolar epithelial cells (HPAEpiC). An analysis of clinical serum samples revealed increased levels of miR-205-5p and high mobility group box 1 (HMGB1) after hip fracture. A bioinformatics analysis and dual-luciferase reporter assay identified HMGB1 as a potential target of miR-205-5p. The overexpression of miR-205-5p clearly reduced the expression of HMGB1 and inhibited NF-κB signaling, apoptosis, and proinflammatory cytokine production while enabling continued cell proliferation. Our results demonstrate that the upregulation of miR-205-5p suppresses inflammatory responses and promotes cell viability and proliferation by selectively targeting HMGB1 in the context of lung injury after hip fracture. Therefore, miR-205-5p may be an alternative target of therapeutic strategies for lung injury after hip fracture.
Highlights
Hip fracture is a common type of bone fracture in the elderly and is associated with high rates of mortality and a high incidence of complications that mainly result from immune disorders [1]
hematoxylin and eosin (H&E) staining of lung tissue sections revealed the main histologic differences in the hip fracture group relative to control group, including neutrophil marginalization around the lobules and cellulose-like necrosis in the arteries
To explore the inflammatory responses in the SD rat model of hip fracture, we examined the concentrations of IL6 and high mobility group box 1 (HMGB1) in serum samples via enzymelinked immunosorbent assays (ELISAs)
Summary
Hip fracture is a common type of bone fracture in the elderly and is associated with high rates of mortality and a high incidence of complications that mainly result from immune disorders (e.g., rapid inflammatory response) [1]. The trauma associated with surgery, which is the current standard treatment strategy for hip fracture, could induce posttraumatic systemic inflammation and subsequent remote organ damage. Lung infection is the most common postoperative complication and has been associated with high hospitalization and mortality rates [5,6,7,8]. Improvements in surgical techniques and hospital care and advanced prevention strategies have led to reductions in the incidence of complications after hip fracture, the risk of infectious and inflammatory lung injury after hip fracture remains very high [9]. Improvements in surgical techniques and hospital care and advanced prevention strategies have led to reductions in the incidence of complications after hip fracture, the risk of infectious and inflammatory lung injury after hip fracture remains very high [9]. erefore, a detailed exploration of the molecular mechanisms involved in the progression of lung injury after hip fracture and the identification of a critical mediator as a potential therapeutic target in such cases are highly important
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