ArticleMolecular therapy. Nucleic acids2023
miR-342-5p downstream to Notch enhances arterialization of endothelial cells in response to shear stress by repressing MYC.
Article in Molecular therapy. Nucleic acids, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 5 citations in OpenAlex.
- Laminar Flow Alters EV Composition in HUVECs: A Study of Culture Medium Optimization and Molecular Profiling of Vesicle Cargo.Small methods · 2025Article
- Article
- Under pressure: integrated endothelial cell response to hydrostatic and shear stresses.Vascular biology (Bristol, England) · 2025Article
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14 authors at 3 institutions in 1 country.
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Abstract
During vascular development, endothelial cells (ECs) undergo arterialization in response to genetic programs and shear stress-triggered mechanotransduction, forming a stable vasculature. Although the Notch receptor is known to sense shear stress and promote EC arterialization, its downstream mechanisms remain unclear. In this study, the Notch downstream miR-342-5p was found to respond to shear stress and promote EC arterialization. Shear stress upregulated miR-342-5p in a Notch-dependent manner in human umbilical vein endothelial cells (HUVECs). miR-342-5p overexpression upregulated the shear stress-associated transcriptomic signature. Moreover, miR-342-5p upregulated arterial markers and promoted EC arterialization in a Matrigel plug assay and retinal angiogenesis model. In contrast, miR-342-5p knockdown downregulated arterial markers, compromised retinal arterialization, and partially abrogated shear stress and Notch activation-induced arterial marker upregulation. Mechanistically, miR-342-5p overexpression suppressed MYC to repress EC proliferation and promote arterialization, achieved by promoting MYC protein degradation by targeting the EYA3. Consistently, EYA3 overexpression rescued miR-342-5p-mediated MYC downregulation and EC arterialization.
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