ArticleSaudi journal of biological sciences2019
Application of high-fat cell model in steady-state regulation of vascular function.
Article in Saudi journal of biological sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- Irisin: A Potentially Fresh Insight into the Molecular Mechanisms Underlying Vascular Aging.Aging and disease · 2023Review
- Small molecule compound M12 reduces vascular permeability in obese mice via blocking endothelial TRPV4-Nox2 interaction.Acta pharmacologica Sinica · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
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Abstract
In order to effectively apply the high-fat cell model to the regulation of vascular homeostasis and the repair of vascular endothelial cell injury, and to provide a new theoretical basis for the treatment of vascular homeostasis imbalance in the future, in this study, the mouse thoracic aorta tissue is extracted by using mouse endothelial cells. Western blotting and immunofluorescence resonance energy transfer (Immuno-FRET) are then used to verify the distribution and physical coupling properties of TRPV4 and Nox2 in cells. Finally, mouse mesenteric endothelial cells are isolated and cultured to induce FFA high-fat cell model. The results show that the nucleic acid expression levels of TRPV4 and Nox2 in RNA are significantly different from those of TRPV4 and Nox2 in protein. The relative values of TRPV4 and Nox2 in the control group are relatively low (0.8 ± 0.11). However, the relative values of TRPV4 and Nox2 are higher in the FFA high-fat cell model induced by the experimental group, and the values are (1.7 ± 0.8). Obviously, the relative values of TRPV4 and Nox2 in the experimental group are higher than those in the control group. The expression of reactive oxygen species (ROS) in vascular endothelial cells of control group is (1.0 ± 0.16), and that in FFA group is (2.5 ± 0.46). The expression of ROS in FFA cell model with HC067047A inhibitor is (1.5 ± 0.38). In the FFA cell model with apo inhibitor, ROS expression is (1.2 ± 0.23). Thus, in the FFA high-fat cell model induced successfully, the physical coupling of TRPV4 and Nox2 increases in primary endothelial cells, and the increase of physical coupling of TRPV4 and Nox2 results in the increase of ROS expression, which also means the imbalance of ROS homeostasis in vascular endothelial cells and the change of vascular endothelial cell permeability. The expression levels of TRPV4 and Nox2 are used as indicators of whether the vascular function is stable or unbalanced, thus providing a new theoretical basis for the treatment of cardiovascular diseases.
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