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RNF6 Targeted by miR-26a-5p Protects Pancreatic β-Cell Function Against Type 2 Diabetes

BACKGROUND: Type 2 diabetes (T2D) is characterized by progressive β-cell dysfunction. Regulatory microRNAs (miRNAs) may be associated with this. METHODS: Serum miR-26a-5p and RNF6 levels were detected in T2D patients and healthy volunteers via qRT-PCR. Subsequently, the role of specific dysregulated...

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Detalles Bibliográficos
Autores principales: Yang, Fan, Zhao, Shengxun, Zhang, Xuyan, Ding, Sheng, Xu, Yancheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8761081/
https://www.ncbi.nlm.nih.gov/pubmed/35046680
http://dx.doi.org/10.2147/DMSO.S335088
Descripción
Sumario:BACKGROUND: Type 2 diabetes (T2D) is characterized by progressive β-cell dysfunction. Regulatory microRNAs (miRNAs) may be associated with this. METHODS: Serum miR-26a-5p and RNF6 levels were detected in T2D patients and healthy volunteers via qRT-PCR. Subsequently, the role of specific dysregulated miR-26a-5p or RNF6 in regulating insulin content, cell proliferation, and apoptosis was studied in INS-1 cells. The targeting correlation between miR-26a-5p and RNF6 was detected using a luciferase assay. RESULTS: RNF6 expression was significantly decreased in T2D individuals and INS-1 cells treated with high glucose, while miR-26a-5p expression was increased. In INS-1 cells, RNF6 overexpression or miR-26a-5p downregulation significantly increased insulin content and secretion, induced proliferation, and inhibited apoptosis. RNF6 has been identified as an miR-26a-5p target, which negatively regulates RNF6 to worsen INS-1 cell function. CONCLUSION: RNF6 promoted insulin secretion and induced cell proliferation in INS-1 cells. This may be related to miR-26a-5p targeting and negatively regulating T2D pathogenesis.