Frontiers in cell and developmental biology · 2026
Impact of acute stress on gastric interstitial cells of Cajal disorder.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Huang Zhen-Peng, Wang Ke, Qiu Hu, Wan Ji-Wei, Yang Zhi, Kong Ling-Wang, Li Zhuo-Yuan
Аннотация
INTRODUCTION: Acute stress can disrupt gastrointestinal function. Interstitial cells of Cajal (ICCs) regulate gastric motility; however, the effects underlying their alterations during stress remain unclear. We aimed to explore the potential impact of acute stress on alterations in gastric ICCs.
METHODS: Animals were assigned to one control and four study groups (0, 24, and 72 h). Acute stress was induced via right chest puncture using a Hopkinson bar. Lung injury was assessed using hematoxylin-eosin staining, gastric ICCs were examined using immunohistochemistry, immunohistofluorescence, and TdT-mediated dUTP nick-end labeling assays. Transmission electron microscopy was used to evaluate ultrastructural changes. Western blotting and real-time polymerase chain reaction were used to analyze SCF/c-kit, protein 53 (p53), and the Wnt/β-catenin signaling pathways. Enzyme-linked immunosorbent assay was used to quantify nuclear factor kappa B (NF-κB) p65, interleukin (IL)-1β, IL-6, IL-9, IL-10, tumor necrosis factor-alpha (TNF-α), and cortisol. Spectrophotometry was used to determine the levels of reactive oxygen species (ROS) and malondialdehyde (MDA).
RESULTS: The lung tissue exhibited congestion, edema, and the destruction of the alveolar structure following puncture. The gastric ICCs tested positive for the surface markers CD117/c-kit and CD34. The population and apoptosis of the gastric ICCs were altered in the acute stress condition. Moreover, acute stress caused dysregulated SCF/c-kit, Wnt/β-catenin, p53 and NF-κB pathways. IL-1β, IL-6, IL-9, IL-10, TNF-α, and cortisol demonstrated altered expression levels, whereas ROS and MDA were upregulated in the acute stress condition.
CONCLUSION: Acute stress damages gastric ICCs through the Wnt/β-catenin, JAK/STAT, and NF-κB signaling pathways, as well as p53-and SCF/c-kit pathway-mediated abnormalities and oxidative stress, contributing to functional alterations in gastric ICCs.
METHODS: Animals were assigned to one control and four study groups (0, 24, and 72 h). Acute stress was induced via right chest puncture using a Hopkinson bar. Lung injury was assessed using hematoxylin-eosin staining, gastric ICCs were examined using immunohistochemistry, immunohistofluorescence, and TdT-mediated dUTP nick-end labeling assays. Transmission electron microscopy was used to evaluate ultrastructural changes. Western blotting and real-time polymerase chain reaction were used to analyze SCF/c-kit, protein 53 (p53), and the Wnt/β-catenin signaling pathways. Enzyme-linked immunosorbent assay was used to quantify nuclear factor kappa B (NF-κB) p65, interleukin (IL)-1β, IL-6, IL-9, IL-10, tumor necrosis factor-alpha (TNF-α), and cortisol. Spectrophotometry was used to determine the levels of reactive oxygen species (ROS) and malondialdehyde (MDA).
RESULTS: The lung tissue exhibited congestion, edema, and the destruction of the alveolar structure following puncture. The gastric ICCs tested positive for the surface markers CD117/c-kit and CD34. The population and apoptosis of the gastric ICCs were altered in the acute stress condition. Moreover, acute stress caused dysregulated SCF/c-kit, Wnt/β-catenin, p53 and NF-κB pathways. IL-1β, IL-6, IL-9, IL-10, TNF-α, and cortisol demonstrated altered expression levels, whereas ROS and MDA were upregulated in the acute stress condition.
CONCLUSION: Acute stress damages gastric ICCs through the Wnt/β-catenin, JAK/STAT, and NF-κB signaling pathways, as well as p53-and SCF/c-kit pathway-mediated abnormalities and oxidative stress, contributing to functional alterations in gastric ICCs.