Oxidative stress-induced miR10b disrupts endothelial cell function

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  • 血管内皮細胞におけるストレス応答性miR10bの機能解析

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Abstract

Endothelial cells (ECs) are constantly exposed to environmental stress factors that trigger cellular senescence and apoptosis. The altered EC function is related to the progression of age-related diseases, such as Alzheimer’s disease. We have identified that microRNA10b (miR10b) is upregulated in ECs following oxidative stresses, however, the biological function of miR10b in ECs is poorly understood. Overexpression of miR10b in human umbilical vein endothelial cells (HUVECs) decreased EC proliferation and tube formation. Conversely, addition of miR10b inhibitor increased EC proliferative ability. Furthermore, overexpression of miR10b suppressed protein expression of VE-cadherin (VE-cad), an endothelial adhesion molecule, and altered VE-cad localization at adherens junctions. We also found that ferulic acid, a polyphenol derived from natural plants, inhibited the induction of miR10b by oxidative stress stimulation, thereby protecting ECs from apoptosis. These results suggest that miR10b contributes to disruption of VE-cad-based junctions induced by oxidative stress, therefore, targeting miR10b may be a promising biomarker capable of detecting EC dysfunctions.

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  • 医療工学雑誌

    医療工学雑誌 (18), 1-8, 2024-03-15

    広島国際大学大学院　医療・福祉科学研究科　医療工学専攻

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