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  • Author or Editor: L. Liu x
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Abstract

Although the use of aspirin has substantially reduced the risks of cardiovascular events and death, its potential mechanisms have not been fully elucidated. In a previous study, we found that aspirin triggers cellular autophagy. In the present study, we aimed to determine the protective effects of aspirin on human coronary artery endothelial cells (HCAECs) and explore its underlying mechanisms. HCAECs were treated with oxidized low-density lipoprotein (ox-LDL), angiotensin II (Ang-II), or high glucose (HG) with or without aspirin stimulation. The expression levels of endothelial nitric oxide (NO) synthase (eNOS), p-eNOS, LC3, p62, phosphor-nuclear factor kappa B (p-NF-κB), p-p38 mitogen-activated protein kinase (p-p38 MAPK), and Beclin-1 were detected via immunoblotting analysis. Concentrations of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were measured via ELISA. NO levels were determined using the Griess reagent. Autophagic flux was tracked by tandem mRFP-GFP-tagged LC3. Results showed that aspirin increased eNOS level and reduced injury to the endothelial cells (ECs) caused by ox-LDL, Ang-II, and HG treatment in a dose-dependent manner. Aspirin also increased the LC3II/LC3I ratio, decreased p62 expression, and enhanced autophagic flux (autophagosome and autolysosome puncta) in the HCAECs. p-NF-κB and p-p38 mitogen-activated protein kinase inhibition, sVCAM-1 and sICAM-1 secretion, and eNOS activity promotion by aspirin treatment were found to be dependent on Beclin-1. These results suggested that aspirin can protect ECs from ox-LDL-, Ang-II-, and HG-induced injury by activating autophagy in a Beclin-1-dependent manner.

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In the past decade, researches on Wnt signaling in cell biology have made remarkable progress regarding our understanding of embryonic development, bone formation, muscle injury and repair, neurogenesis, and tumorigenesis. The study also showed that physical activity can reverse age-dependent decline in skeletal muscle, preventing osteoporosis, regenerative neurogenesis, hippocampal function, cognitive ability, and neuromuscular junction formation, and the age-dependent recession is highly correlated with Wnt signaling pathways. However, how the biological processes in cell and physical activity during/following exercise affect the Wnt signaling path of the locomotor system is largely unknown. In this study, we first briefly introduce the important features of the cellular biological processes of exercise in the locomotor system. Then, we discuss Wnt signaling and review the very few studies that have examined Wnt signaling pathways in cellular biological processes of the locomotor system during physical exercise.

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