ArticleActa diabetologica2026
miR-142-3p overexpression targets CLTA and impairs clathrin-mediated endocytosis in HLSECs induced by high glucose.
Article in Acta diabetologica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveThis study aims to explore the effect of miR-142-3p on the endocytosis in human liver sinusoidal endothelial cells (HLSECs) induced by high glucose and to investigate the underlying mechanisms.
methodsMulti-database target prediction was performed to identify potential targets of hsa-miR-142-3p. HLSECs were cultured under 5.5 mmol/L glucose (normal) or 25 mmol/L glucose (high) conditions. qRT-PCR assessed the RNA expression levels of miR-142-3p and CLTA. Western blot assessed the protein expression levels of clathrin-mediated endocytosis(CME)-related genes. Immunofluorescence assay was used to observe the cellular localization of CLTA. A dual-luciferase assay investigated the targeting relationship between miR-142-3p and CLTA. DiI-LDL endocytosis assay was used to study the endocytosis in HLSECs.
resultsBioinformatics analysis predicted CLTA as a potential target of miR-142-3p. The expression level of miR-142-3p was increased and the expression levels of CLTA, α-adaptin, AP2M1 and VPS35 were reduced in high glucose-induced HLSECs (P < 0.05). DiI-LDL endocytosis assay demonstrated that the endocytosis was weakend in HLSECs induced by high glucose. Dual-luciferase reporter assay confirmed that miR-142-3p directly targets CLTA. Compared with the negative control group, inhibition of miR-142-3p significantly increased the expression levels of CLTA, AP2M1, α-adaptin and VPS35, and improved the endocytosis in HLSECs (P < 0.05). In contrast, overexpression of miR-142-3p showed the opposite effects.
conclusionsmiR-142-3p overexpression targets CLTA and impairs CME in HLSECs induced by high glucose. The concurrent changes in other CME-related genes further suggest a broader regulatory role of miR-142-3p on the endocytosis.
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